| JOURNAL HOME | CME HOME | THIS MONTH | PAST ISSUES | ETOC | COLLECTIONS |
| AUTHORS | REVIEWERS | EDITORIAL BOARD | FEEDBACK | RSS | HELP |
| ||||||||||||||
| ||||||||||||||
|
|
|
|
||||||||||||
|
||||||||||||||
From the Departments of Anesthesia and Surgery; Rhode Island Hospital, Providence Rhode Island; Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts
Address correspondence and reprint requests to Andrew Maslow, MD, Department of Anesthesiology, Rhode Island Hospital, Davol 129, 593 Eddy St, Providence, RI 02903. Address email to amaslow{at}lifespan.org
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionConclusionsReferences |
|---|
IMPLICATIONS: Compared with placebo, both epinephrine and milrinone similarly improved biventricular performance after aortic valve replacement, with a greater impact on right ventricular function. Choice of either inotropic drug should be driven by blood pressure and hemodynamic goals in this setting.
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsReferences |
|---|
Although one investigation identified a subset of patients with AS undergoing AVR with a greater requirement for inotropes, other data have identified patients believed to be at increased risk for LVOTO with the use of inotropes and vasodilators (6–8). Neither study assessed the risks and benefits of inotropes in a randomized fashion, nor has the risk of LVOTO been assessed immediately after cardiopulmonary bypass (CPB) (6–8). The purpose of this study was to assess the effects of epinephrine and milrinone on biventricular function immediately after AVR for AS. We hypothesize that IV milrinone and epinephrine will improve hemodynamics, compared with placebo, immediately after AVR without increased risk of LVOTO.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsReferences |
|---|
1.0 cm2) scheduled for elective AVR. Presenting symptoms included congestive heart failure (CHF), presyncope, syncope, dyspnea, and/or fatigue. All patients had less than moderate aortic insufficiency. Patients were randomized to one of three study groups: epinephrine, milrinone, or placebo. Milrinone and epinephrine represent two different classes of inotropes, the former being a phosphodiesterase inhibitor with significant vasodilatory and lusitropic effects associated with its inotropic effects, and the latter being a ß agonist with a greater tendency to increase vascular tone in association with its inotropic effects. The selection of milrinone over other phosphodiesterase inhibitors is based on its clarity, allowing the drugs to be administered in a blinded fashion. Patients with significant single vessel coronary artery disease requiring coronary artery bypass grafting (CABG) were included if the coronary artery narrowing was a secondary finding during cardiac catheterization and was not considered the primary reason for patient presentation. These patients had no anginal symptoms or evidence of a myocardial infarction (MI) (by electrocardiography) related to the coronary artery narrowing nor any focal systolic wall abnormalities during echocardiographic examination. However, global dysfunction may have been present. Patients with two or more coronary vessel disease or who presented with symptoms of angina were excluded. Patients with any coronary artery narrowing that was directly associated with a MI were excluded.
Patients with additional significant coexisting valve disease (more than moderate mitral or more than mild tricuspid valve regurgitation or stenosis, or for which valve replacement or repair was planned or performed) or those with previously documented nonvalvular LVOTO were excluded. The absence of these exclusions was confirmed by initial intraoperative echocardiographic evaluation.
All patients had sinus rhythm before CPB. After CPB patients had either sinus rhythm or were electronically paced to maintain atrial-ventricular sequential rhythm at a rate of approximately 90 bpm.
Management of Surgical Procedure
Induction of anesthesia consisted of thiopental, pancuronium, and fentanyl. Administration of benzodiazepines was at the discretion of the attending anesthesiologist. Maintenance of anesthesia was accomplished using fentanyl, pancuronium, isoflurane (<1%), and oxygen. Normocarbia was maintained throughout the surgical procedure. Ventilation was adjusted to maintain normocarbia (35–45 mm Hg) and normal pH (7.35–7.45). Data were obtained during brief periods of apnea. The hematocrit (Hct) was maintained more than 24%.
Monitoring consisted of the standard noninvasive monitors along with an intraarterial catheter and a pulmonary artery catheter (Right Ventricular Ejection Fraction Catheter; Baxter Edwards, Irvine CA). The pulmonary artery catheter and transesophageal echocardiography probe were placed after the induction of general anesthesia. Proper catheter position was achieved using continuous right atrial and pulmonary artery port wave form monitoring.
All surgical procedures were performed by the same surgeon (AKS). CPB was performed using a closed system membrane oxygenator with centrifugal pumps with normothermic perfusate at 37°C. Before placement of aortic and right atrial cannulae, anticoagulation was achieved with 3–4 mg/kg heparin to achieve an activated clotting time (ACT) >450 s. The extracorporeal circuit was primed with 500 mL hetastarch, 1400 mL plasmalyte, mannitol (12.5 gm), and 50 meq of sodium bicarbonate. The flow rate was maintained at 2.5 L · min-1 · m-2. There was a single period of aortic cross-clamping (AoXCl) during which the surgical procedure was performed. Intermittent cold antegrade crystalloid and blood cardioplegia were delivered into the aortic root. The heart was topically cooled using ice-cold saline. Hcts were maintained at more than 21% during CPB and then >25% after separation from CPB. Systemic vascular resistance (SVR) was maintained using a vasopressor (phenylephrine) or vasodilator (isoflurane) to sustain a mean arterial blood pressure (MBP) between 60–80 mm Hg measured in the aorta via aortic cannula while on CPB.
The cardioplegia technique was as follows: after placement of the AoXCl, cardioplegia was administered antegrade to achieve cardiac standstill (electrical silence by electrocardiography). Thereafter, cardioplegia was administered via cannula placed under direct vision in the left main and right coronary arteries intermittently every 15 min to maintain electrical silence. Terminal perfusion pressure was as high as 80 mm Hg. Retrograde cardioplegia was not used in any patient.
The initial dose was 900 mL of cold (2°C) crystalloid cardioplegia. The solution consists of 1000 mL of a 5% dextrose solution consisting of 27 meq of sodium chloride, 30 meq potassium chloride, 3 meq of magnesium sulfate, and THAM (tris-hydroxy amino-methamine) to buffer the solution to 7.7.
Subsequent doses were 400 mL of cold blood cardioplegia. The solution consisted of 1000 mL of cold (13°C), oxygenated (PO2 approximately 200 mm Hg), hemodiluted blood (Hct 22%–25%), supplemented with 20 meq of potassium chloride, sodium citrate, phosphate, dextrose, and THAM. Nitroglycerin (0.2 mL of a 5 mg/mL concentration) was added to the blood cardioplegia.
For those patients in whom a coronary artery was bypassed, the distal anastomosis was performed before AVR and the proximal anastomosis (vein grafts) was performed after closure of the aortotomy. Once the distal anastomosis was completed a dose of cardioplegia was administered via the vein graft. The type of prosthetic valve placed was determined by the surgeon (AKS) along with the patient.
After successful separation from CPB, protamine (1.5 mg per mg of the initial heparin dose) was administered to neutralize the anticoagulant effects of heparin. Additional protamine (1 mg/kg) was given for persistently increased ACT (>20% baseline) until a normal ACT (<20% baseline) was achieved or until up to 7 mg/kg of protamine had been given.
Protocol
Study drugs were prepared by a separate investigator, and the infusion labels were covered, then given to the primary anesthesiologist so that the surgeon and anesthesiologist were blinded as to which drug the patient was to receive. Study medicines were administered immediately after the removal of the AoXCl and before separation from CPB. The milrinone group received an initial loading dose of 30 µg/kg of IV milrinone (200 µg/mL) given over 10 min, followed by a continuous IV infusion of 0.30 µg · kg-1 · min-1. Although larger initial loading doses and infusion regimens have been advocated for milrinone, concerns of hypotension and an increased need for vasoconstrictor prompted the use this smaller dose (9–11). The epinephrine group received an equivalent bolus of saline (NS) over 10 min followed by a continuous IV infusion of epinephrine of 30 ng · kg-1 · min-1. The placebo group received an equivalent volume of NS as an initial loading dose followed by a continuous infusion of NS at a rate equal to that of the study drugs. All drug infusions were administered using 100 mL solutions: 100 mL of pre-prepared milrinone (20 mg); 1 mg of epinephrine in 100 mL NS solution; 100 mL NS mean systemic blood pressure (MBP) solution.
Hemodynamic and echocardiographic data were obtained at the following time points:
Different investigators obtained data simultaneously. While one investigator obtained echocardiographic data, another obtained data from the pulmonary artery catheter. All data were obtained during brief periods of apnea. Measurements were made in triplicate and averaged to yield a mean.
Hemodynamic goals, as per our routine, include a cardiac index (CI) 
2.5 L · min-1 · m-2, systemic blood pressure (SBP) > 90/50 mm Hg, pulmonary artery pressures (PAP) 40/25 mm Hg, and a heart rate <110 bpm. During the study period, a vasopressor (phenylephrine) was administered for MBP <90/50 mm Hg when CI was more than 2.5 L · min-1 · m-2. A vasodilator (nitroglycerin) was administered for SBP more than 130/85 mm Hg. After collection of all study data, an inotrope was administered if the CI was low and the PAP were increased. The choice of inotrope was at the discretion of the attending anesthesiologist, consistent with our typical clinical practice.
Data
Age, gender, body surface area, preoperative medications, presence of hypertension, presence of LV hypertrophy (based on preoperative transthoracic echocardiography; LV wall thickness > 11 mm), preoperative aortic valve area, and patient presentation (CHF, MI, syncope, decrease exercise capacity, or fatigue) were recorded. CHF or pulmonary edema was diagnosed based on the presence of chest examination demonstrating rales, and/or by interpretation of the patient’s chest radiograph showing signs of pulmonary edema. MI was diagnosed based on two of the four following symptoms or signs; angina, electrocardiography evidence of focal abnormality, increase of cardiac enzymes, and/or presence of a focal systolic wall motion abnormality on echocardiogram. Pre-syncope or syncope is defined as dizziness, lightheadedness, or loss of consciousness. Reduced exercise tolerance or fatigue was based on the patients’ subjective and/or objective reporting of their own abilities. Surgical data included surgical procedure, times for AoXCl and CPB.
Heart rate (HR; all patients had atrioventricular synchrony), mean systemic blood pressure (MBP), right atrial pressure (RAP), mean PAP (mPAP), pulmonary capillary wedge pressure (PCWP), cardiac output (CO), and CI were recorded. Right ventricular systolic and diastolic volumes (RVEDV) and ejection fraction (RVEF) were measured using a RVEF catheter (Baxter Edwards). These data were obtained with a thermodilution technique using room temperature dextrose solution. Measurements were made in triplicate during brief periods of apnea and averaged. Only diastolic volume and ejection fraction (EF) are reported. Systemic and pulmonary vascular resistances (SVR and PVR) were calculated. Stroke volumes were also obtained.
Left ventricular systolic (LVESD) and diastolic (LVEDD) diameters and LVEF were measured from the transgastric short axis window at the mid-papillary muscle level using the Teichholz equation. Only LVEDD and EF are reported. Transmitral (peak E and A velocities, deceleration, and isovolumic relaxation times) and pulmonary venous (peak systolic [S] and diastolic [D] inflow velocities) flow profiles were obtained to assess left sided diastolic function. Assessment of diastolic function was based on patterns reported in previous literature and summarized in Table 1 (12,13).
|
2.0 m/s, and/or by the appearance of a "dagger" shaped flow velocity profile. Hemodynamic and echocardiographic data were combined to assess pressure volume relationships during diastole allowing additional assessment of ventricular diastolic function. RAP was combined with RVEDV (RAP/RVEDV) and PCWP was combined with LVEDD (PCWP/LVEDD). After sternal closure, ventricular preload was increased by changing the patient position from supine to 35 degrees Trendelenburg. Pressure and volume measurements were then reassessed and recorded.
Demographic, presurgical, surgical and pre-CPB hemodynamic and echocardiographic variables were compared among groups using Kruskal-Wallis tests or using Fisher’s exact test for categorical variables. Post-CPB hemodynamic and echocardiographic variables, or the changes in these variables from pre- to post-CPB, as well as measures of ventricular compliance with fluid administration, were compared among groups using Kruskal-Wallis tests. Median values are reported in the text. The associations between variables were assessed using Spearman correlation coefficients. Two-sided P values <0.05 were considered as statistically significant. SAS v8.2 (SAS Institute Inc., Cary, NC) was used for the statistical analysis.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsReferences |
|---|
Echocardiographic evaluation before and after CPB did not demonstrate any additional valve dysfunction (aside from the AS) defined as more than or equal to moderate severity in stenosis or regurgitation. Two-dimensional and Doppler echocardiographic analyses of the LVOT and aortic valve confirmed AS before CPB. After separation from CPB two-dimensional and Doppler echocardiographic analysis revealed normal prosthetic valve function and no evidence of abnormal flow velocities/profile (AFV) or LVOTO for all patients (95% confidence interval; 0%–14%). The reported incidence of AFV after AVR without inotropes or dilators is 14% and 30%–48% after administration of inotropes and dilators (6,7).
Hemodynamic data are presented in Tables 2–4 and Figure 1. Baseline hemodynamic data were similar among the three study groups. Patients in both the epinephrine and milrinone groups had greater CO (5.7 L/min, 6.2 L/min, respectively; P = 0.005) and CI (2.8 L · min-1 · m-2, 3.0 L · min-1 · m-2, respectively; P = 0.04) immediately after CPB compared with the placebo group (4.5 L/min and 2.4 L · min-1 · m-2) with correspondingly larger increases in CO from pre to post CPB (epinephrine, +1.70 L/min; milrinone, +1.74 L/min; and placebo, +0.71 L/min; P = 0.03). The change in PVR from pre- to post-CPB was significantly different for the placebo group (+18 dynes · s/cm5) compared with the epinephrine and milrinone groups (-64 and -74 dynes · s/cm5 respectively; P = 0.01).
|
|
|
|
We observed that changes in LVEF were not significantly correlated with changes in CO or CI (r = 0.22; r = 0.08 respectively); however, changes in RVEF were positively correlated with CO (r = 0.56; P < 0.001), and CI (r = 0.47; P < 0.01). We also observed that changes in LVEF and changes in RVEF were moderately and statistically significantly correlated (r = 0.35; P = 0.04).
The effects of fluid administration are illustrated in Table 5. There were no statistically significant differences among the three groups in changes in PCWP/LVEDD with fluid administration. There was a significant correlation between changes in PCWP/LVEDD and change in RAP/RVEDV (r = 0.59; P < 0.001).
|
Pre-CPB LVEF was predictive of post-CPB LVEF. Adjusting for pre-CPB LVEF did not affect the significance of the benefit seen with inotropes on changes in LVEF or RVEF. Pre-CPB LVEF was also not correlated with changes in PCWP/LVEDD during fluid administration.
There are positive correlations between changes in RVEF from pre- to post-CPB and pre-CPB mPAP (r = 0.32) and pre-CPB PVR (r = 0.61). However, when a regression model is applied to account for each of these correlations, there is still a significant effect of inotropes on change in RVEF, so the change in RVEF cannot be attributed to the pre-CPB PVR or mPAP.
There were no significant differences with respect to transmitral and pulmonary venous flows before or after CPB. All three groups had similar numbers of patients with normal and abnormal patterns of diastolic function before and after CPB. Ninety-one percent of patients receiving inotropes and 75% of placebo patients had abnormal diastolic function before CPB. After CPB these numbers decreased to 72% and 58%, respectively.
All patients had CI more than 2.0 L · min-1 · m-2 immediately after separation from CPB. After all data were collected, 6 patients in the placebo group (4 milrinone or amrinone; 2 epinephrine), and 1 patient in the milrinone group (epinephrine) were given inotropes for CI <2.5 L · min-1 · m-2 as decided by the primary anesthesiologist and/or the surgical attending. No patient in the epinephrine group received additional inotropes. After the administration of additional inotropic therapy a CI more than 2.5 L · min-1 · m-2 was achieved for all 7 patients. Of the 11 patients in the epinephrine groups, 7 (64%) received nitroglycerin at some point during the post-CPB period. Two (18%) and 4 (36%) patients receiving milrinone required nitroglycerin and phenylephrine respectively during the intraoperative period. Three patients in the placebo group received nitroglycerin and 3 received phenylephrine after CPB.
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsReferences |
|---|
Although the data did not demonstrate improved LV diastolic function with the use of inotropes, there was a trend for better RV compliance with the administration of epinephrine. Transmitral and pulmonary venous flow patterns were consistent with abnormal LV diastolic function in more than 75% of patients before CPB, and abnormalities were still present in more than 50% after CPB.
LV systolic function improves immediately after AVR for AS, whereas LV diastolic dysfunction persists (1–5). The increase in LVEF (+5.5%) seen in the placebo group of the present study is similar to that reported after AVR in other investigations (5%–6%) (4,5). Changes in LV diastolic function, however, are variable, ranging from immediate increase in dysfunction to a prolonged recovery over years (1–5). For patients with AS, LV diastolic dysfunction is attributable to myocardial hypertrophy, myocardial fibrosis, and/or ischemia (1,3,4,14–17). Diastolic dysfunction has also been reported after CPB with cardioplegic arrest (14,15,17–21). This is attributable, in part, to myocardial ischemia and edema, both of which may occur with or without significant coronary artery narrowing (17,18,21). Resolution of this myocardial edema can be hastened with the administration of inotropes, but is still present 6 hours after CPB (21). In the present study we did not see any immediate benefit, compared with placebo, on diastolic function with use of inotropes. This may be attributable to the timing and duration of analysis, which was limited to the immediate post-CPB period and which might not have been of sufficient duration to assess changes in diastolic function resulting from myocardial edema. Improvement of chronic LV diastolic dysfunction with the administration of inotropes (compared with placebo) is also not likely to occur immediately after CPB. Although the proper treatment of acute and chronic diastolic function depends on its etiology (e.g., acute ischemia versus cardioplegia-associated myocardial edema), available data support the use of inotropes for such patients in the post-CPB period (21,34).
RV dysfunction has been described after CPB with cardioplegic arrest (8,22–26). In a study of 24 CABG patients with normal LV and RV systolic function before CPB, a reduction in RVEF from 49% to 46% was seen after CPB, reaching a nadir 4 hours after CPB (RVEF 31%), with recovery over the next 8 hours (22–26). During this time the RV has limited reserve to tolerate increases in preload, afterload, and myocardial depressants (22–26).
RV dysfunction has also been reported in a subset of patients with AS scheduled for AVR (8). Patients with preoperative transaortic valve peak gradients >120 mm Hg (Group 2) had significantly lower RVEF at baseline compared with patients with gradients <100 mm Hg (Group 1; RVEF 34% versus 45%). After pericardiotomy Group 2 displayed increases in right heart volumes and RV diastolic pressure, and reductions in RV systolic pressure and RVEF (mean <30%). By contrast, Group 1 displayed little change in these variables. Immediately after CPB both groups recorded similar hemodynamic data and RV function; however, Group 2 received significantly more epinephrine (6.7 µg/min versus 3.2 µg/min). The authors discussed the role of ventricular interdependence to explain the association between the severity of AS and RV dysfunction, suggesting that chronic transmission of high LV cavity pressures across the interventricular septum or pulmonary vasculature contributes to RV dysfunction (8).
Several experimental models of ventricular interdependence demonstrate how changes in right or left heart pressure, size, and/or contractility affect left and right heart function respectively (27–29). Leeuwenburgh et al. (29) reported that acute volume unloading of the LV while maintaining systemic flows and pressures results in increased right heart volumes and decreased RV contractility. Experimental RV failure and dilation results in impairment of both LV systolic and diastolic function (27,28). These results were attributed to alterations in RV geometry and interventricular septal position, suggesting that the septal position is a reflection of the trans-septal volume and/or pressure gradients (8,27–29). Although the septal shifts are known to affect the diastolic filling of the abutting heart chamber, "the end diastolic position of the septum [also] influences septal motion during systole" (27,28). Decompression of the dilated RV restored RV geometry and returned the ventricular septum toward its normal position, which improved both RV and LV diastolic and systolic function (27–29).
Investigators have reported an increased risk for LVOTO after AVR for AS, (6,7). Aside from case reports, there are no data assessing the risk of LVOTO immediately after CPB (6,7,30,31). Of 53 consecutive patients studied 6–7 days after AVR, 13 (24%) had Doppler echocardiographic evidence of abnormal, dagger-shaped (consistent with dynamic outflow tract obstruction), and high velocity LV systolic outflow (6). In another study, 100 consecutive patients were assessed using Doppler echocardiography 7 days (range, 2–10 days) after AVR for AS (7). Abnormal systolic flow velocity was seen in 14 (14%) patients at rest, and 30% and 48% of patients during the administration of sodium nitroprusside (25 of 93) and dobutamine (37 of 96) respectively. Approximately three-quarters occurred in the midventricular cavity; the remainder occurred in the outflow tract. For these patients, greater pulmonary and hemodynamic dysfunction, longer hospital stays, and increased mortality were associated with AFV (6,7). Case reports have described LVOTO immediately after AVR causing hemodynamic instability (30,31). Intraoperative transesophageal echocardiography had not been used until after these patients had hemodynamic instability (30,31). These reports indicate that small hypertrophied (asymmetric or symmetric) LV cavities, and normal or supernormal EFs, with or without mitral annular calcification are risk factors for AFV after AVR for AS (6,7,30,31). Asymmetric septal hypertrophy has been reported in <10% of patients with AS, and is either a response to the stenotic valve or a result of the coexistence of hypertrophic cardiomyopathy (32). The data from the present study are the first to assess the risk of LVOTO immediately after AVR. The absence of LVOTO in the epinephrine and milrinone groups offers support for the safe use of inotropes in this patient population.
The controversy, therefore, involves the use of inotropic medications for patients with diastolic dysfunction, ventricular hypertrophy, a normal LVEF, and/or anticipated increases of LVEF, who are believed to be at increased risk for LVOTO (1,6,7,30,31). The concept of "isolated diastolic dysfunction" has been questioned. Tissue Doppler analysis has demonstrated myocardial strain and longitudinal ventricular systolic dysfunction, despite a measured LVEF >60%, in hypertensive patients with LV hypertrophy (LVH) (33). Although not studied, it is likely that patients with AS and LVH also have abnormal longitudinal systolic contraction despite a normal LVEF. Basing the decision to administer inotropes on the LVEF ignores these new data, and the importance and impact of RV function and LV diastolic function on hemodynamics and patient outcome (22–28,34,35). Stabilization or improvement of RV function improves LV filling and biventricular function, which is especially important early after CPB when the RV has limited reserve function and LV diastolic dysfunction may be present (8,22–28). Finally, the increased risk of LVOTO immediately after CPB was not supported by the data presented in this study; however, the routine use of echocardiography for its evaluation is still recommended by the authors to assess risk for, and/or allow prompt diagnosis of, LVOTO. Patients who appear to "require" inotropes 48 hours after AVR for AS may benefit from evaluation with echocardiography to assess ventricular function and for abnormal ventricular systolic outflow (6,7).
One limitation of this investigation is the number of patients studied. As there are a number of variables contributing to cardiac performance including the wide range of diastolic function among this patient population, it is difficult to know how much these variables affected the results, especially with the small number of patients studied. Nevertheless, the improvement in hemodynamic measures was consistent for patients receiving inotropes.
One potential bias is generated by the use of transesophageal echocardiography for clinical management as well as collection of study data. Because all study data were collected during a stable period and before any decision to administer additional inotropic medications, we are of the opinion that this variable was minimized.
In the present study, measurements of LVEF and LV dimensions were performed from the transgastric short-axis mid-papillary muscle view using the Teichholz method. This technique is relatively crude and makes assumptions regarding the shape and function of the entire ventricle based on one echocardiographic window. Arguably, formulas (e.g., Simpson’s formula) obtained from multiple echocardiographic windows offer a greater three-dimensional impression of ventricular function. These data are especially more accurate for patients with non-uniformly functioning ventricles. However, data comparing the Teichholz method with more complicated echocardiographic techniques and nuclear imaging have shown that the simpler Teichholz method is accurate for ventricles without systolic wall motion abnormalities, as was the case in the present study (36,37). Furthermore, measurements obtained from the transgastric mid-papillary level are easy to obtain and reproducible, potentially allowing more accurate comparisons within the same patient from one time period to another.
RV function was assessed using the RVEF thermodilution catheter. Numerous in vitro and in vivo studies have demonstrated that the RVEF thermodilution catheter can accurately measure RVEF and volumes when compared with "gold standards" such as biplane and radionuclide angiography (38–40). Accuracy of this catheter is dependent on catheter position (41,42) and the absence of moderate or greater tricuspid regurgitation (43); the latter was not present in any study patient as confirmed during initial transesophageal echocardiography evaluation. During initial placement of the RVEF catheter, right atrial and ventricular waveform monitoring was used to ensure placement of the injectate port just proximal to the tricuspid valve. Spinale et al. (41,42) reported that RVEF measurements remained highly reproducible as long as the injectate port and thermistor positions were within 5 to 10 cm of the tricuspid and pulmonary valves respectively. Continuous catheter port wave form monitoring in our patients ensured that the respective ports remained within these distances during the perioperative period.
The use of high-fidelity intracavitary pressure catheters placed in the ventricles and surface piezoelectric crystals would have given more precise and continuous pressure-volume measurements. These data would have enhanced assessment of ventricular compliance over multiple preload states and allowed measurement of end systolic elastance, a load-independent measure. These more complicated techniques are more easily applied in the laboratory and involve additional manipulations not routinely used during our normal intraoperative management. Although the changes in EF obtained in the present study were consistent within the three groups and with other investigations, our assessment of ventricular compliances would have been significantly improved. It would, therefore, be difficult to state conclusively that inotropes are not beneficial with regard to ventricular compliance based on the data from the present study, especially given the limited time span of the analysis.
|
Conclusions |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsReferences |
|---|
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionsReferences |
|---|
This article has been cited by other articles:
|
|
 |
|
  P. Couture, A. Y. Denault, M. Pellerin, and J.-C. Tardif Milrinone enhances systolic, but not diastolic function during coronary artery bypass grafting surgery: [La milrinone ameliore la fonction systolique mais non la fonction diastolique pendant la chirurgie de pontage aortocoronarien] Can J Anesth, July 1, 2007; 54(7): 509 - 522. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Y. Denault, Y. Lamarche, P. Couture, F. Haddad, J. Lambert, J.-C. Tardif, and L. P. Perrault Inhaled milrinone: a new alternative in cardiac surgery? Seminars in Cardiothoracic and Vascular Anesthesia, December 1, 2006; 10(4): 346 - 360. [Abstract] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
