In cardiovascular anesthesia, cardiac function is commonly monitored by pulmonary artery catheter (PAC) and transesophageal echocardiography (TEE).1–3 However, interpretation of indices derived from PAC and TEE is complicated by their load-dependency.4,5 Especially, measurements of 2-dimensional TEE may be more complicated by the complex structure of the right ventricle (RV).6 Therefore, accurate assessment of RV function is difficult because there are substantial changes in loading conditions and RV geometric structure induced by heart displacement and compression during off-pump coronary artery bypass (OPCAB) surgery.7–9
Previous studies have shown that the end-systolic pressure-volume relations (ESPVR) or its slope, the EES (end-systolic elastance), can reflect myocardial contractile state; and the end-diastolic pressure-volume relations (EDPVR) or its slope, the end-diastolic stiffness (EED), can evaluate passive relaxation properties which contribute to the passive filling phase of the ventricle.10–12
These parameters have also been proven to be relatively independent of loading conditions and very useful for not only the left ventricle but also the right ventricle.13–15 Until recently, to assess ventricular function by end-systolic elastance (EES) and EED, continuous pressure-volume data at various loads under a constant inotropic state were indispensable, which impeded their clinical utility in patients. Although some studies reported that the EES and EED were estimated with pressure-volume data measured from a single-beat, the algorithms of this method were too complicated.16,17 Nonetheless, Steendijk and colleagues18 have previously demonstrated that in addition to the slope of the ESPVR (EES), the position is also a sensitive indicator of changes in contractile state. Accordingly, provided that end-systolic pressure is maintained, a reduced end-systolic volume also indicates an improvement in contractile state. Therefore, according to Steendijk's study,18,19 EES was just estimated by a single ratio of end-systolic pressure divided by end-systolic volume, and EED was also estimated by a single ratio of end-diastolic pressure divided by end-diastolic volume in our study. Consequently, the purpose of this study is twofold: first, to describe and investigate the construction of right ventricular pressure-volume loops (P-V loops) with pressure and volume data measured by a volumetric PAC; second, to evaluate right ventricular systolic and diastolic function by EES and EED in patients who underwent OPCAB surgery. These data may provide reference information for future studies evaluating more complex cardiac status.
This study was conducted between December 2006 and March 2007 with the approval of Human Investigations Committee of Beijing Chaoyang Hospital and patients' written informed consents. The patients were diagnosed with coronary artery disease by coronary angiography preoperatively and scheduled for multivessel OPCAB surgery.
Exclusion criteria were as follows: valvular heart disease on preoperative transthoracic echocardiography (greater than grade I); lack of sinus rhythm on the preoperative electrocardiogram (ECG); moderate or severe abnormality of respiratory function testing preoperatively; concomitant cardiac aneurysm; patients with a pacemaker; hemodynamic instability requiring continuous intra-aortic balloon counter-pulsation (IABP) or inotropic medication perioperatively; conversion to on-pump coronary artery bypass grafting emergently.
Every patient was premedicated with intramuscular 0.1 — 0.2 mg/kg morphine. All patients were routinely monitored with a five lead ECG (II, V5) with ST-segment analysis and pulse oximetry in the operating room. The right radial artery was cannulated for continuous arterial pressure monitoring and blood gas analysis.
Anesthesia was induced with midazolam 0.05 mg/kg, etomidate 0.1 — 0.3 mg/kg, pipecuronium 0.10 — 0.15 mg/kg, sufentanil 1.0 — 2.0 μg/kg and maintained with a continuous infusion of propofol 4—10 mg/kg per hour and intermittent i.v. boluses of pipecuronium 0.05 mg/kg and sufentanil 20 — 40 μg. After tracheal intubation, patients were ventilated at a ventilatory rate of 12 — 16 breaths/min and the ventilatory volume was adjusted to maintain PaCO2 between 35 mmHg and 45 mmHg. A volumetric thermodilution PAC (CCO/CEDV/SvO2 774HF75 type, Edwards Lifesciences, USA) was placed via the right internal jugular vein and connected to an HP monitor (Omnicare24c, Hewlett Packard, USA) and VigilanceTM monitor (Edwards Lifesciences, USA) for hemodynamic measurements.
Isosorbide dinitrate was continuously infused (1 —3 mg/h) throughout the operation. During coronary anastomoses, intravenous fluids and an inotropic agent (dopamine) were used as necessary to maintain mean arterial pressure (MAP) ≥60 mmHg. Only in the case of an urgent decrease in MAP, norepinephrine would be used temporarily with i.v. bolus (10 — 20 μg) to maintain adequate coronary perfusion pressure. When sustained changes of ST-segment occurred (elevation or depression greater than 0.1 mV for more than 60 seconds),20 heart positioning or manipulation was stopped and normalized.
Following median sternotomy, the left internal mammary artery (LIMA) and the saphenous vein, sometimes the left radial artery, were harvested. Before dissection of the LIMA, intravenous heparin 1.5 mg/kg was administered to maintain the activated clotting time >250 seconds. Routine procedures were as follows: the pericardial suture was used to assist exposure of the anastomotic sites; a myocardial stabilizer device was placed to immobilize the area of anastomoses; a coronary shunt was inserted into the target coronary artery to achieve a bloodless surgical field and decrease the ischemic time. The order of grafting were as follows: first, the anastomosis of the LIMA to the left anterior descending coronary artery (LAD) was achieved after exposure of the anterior wall; second, the distal anastomosis of the saphenous vein (sometimes the left radial artery) to the left circumflex coronary artery (LCX) or obtuse marginal artery (OM) was achieved after exposure of the lateral wall; third, the distal anastomosis of the saphenous vein (sometimes the left radial artery) to the right coronary artery (RCA) or posterior descending artery (PDA) was achieved after exposure of the posterior wall. Finally, proximal anastomoses were performed after completion of the distal anastomoses. Shed blood was collected from the surgical field and re-infused with cell saver (BART®2 COBE cardiovascular, USA) during the operation.
The characteristics of patients and operations were recorded. The amount of fluids and dopamine at different time points were recorded. ST-segment changes were recorded.
Hemodynamic data were recorded at the following time points: T1, anesthesia steady-state before skin incision (level before operation); T2, T3, T4, 5 minutes after the stabilizer device was placed for anastomosis on the heart's anterior wall (LAD), lateral wall (LCX or OM), posterior wall (RCA or PDA), respectively; T5, after sternal closure. Mechanical ventilation was held temporarily at each time point to prevent any effect on hemodynamic variables from positive pressure ventilation.
Three sets of data were collected at each time point: first, hemodynamic variables, including CI (cardiac index), SV (stroke volume)/SVI (SV index), RVEF (right ventricular ejection fraction), RVEDV (right ventricular end-diastolic volume)/RVEDVI (RVEDV index), RVESV (right ventricular end-systolic volume)/RVESVI (RVESV index), PAP (pulmonary artery pressure), RAP (right atrial pressure), right ventricular pressure (RVP, see below), PDN (pressure of pulmonary artery dicrotic notch, see below), PVRI (pulmonary vascular resistance index), RVSWI (right ventricular stroke work index), HR (heart rate), PAWP (pulmonary artery wedged pressure), SVRI (systemic vascular resistance index) and MAP, were recorded; second, RV EES was estimated by end-systolic pressure (ESP) divided by ESV, and RV EED was estimated by end-diastolic pressure (EDP) divided by end-diastolic volume (EDV).19 In this study, ESP and EDP corresponded to PDN (see below) and RAP, while RVESVI and RVEDVI were used instead of ESV and EDV. Thus, EES and EED were calculated by the following equation: EES=PDN/RVESVI, EED=RAP/RVEDVI; third, the RV pressure-volume loop was constructed (see below).
Construction of RV pressure-volume loop
It's somewhat difficult to obtain continuous ventricular volume data in the operating room. Nevertheless, there are several specific time-points in the cardiac cycle where pressure and volume may be obtained by a volumetric PAC. These time-points are at end-diastole (end-filling period), end-isovolumic systole, peak-ejection, end-systole (end-ejection period) and end-isovolumic diastole. The acquisition is as follows:
The ventricular volume at end-diastole and end-isovolumic systole corresponds to RVEDV, while that at end-systole and end-isovolumic diastole corresponds to RVESV. RVEDV and RVESV can be recorded directly from the VigilanceTM monitor. Considering the blood pumped from the ventricle was about two-third of SV in the rapid ejection period as a result of myocardial contraction still enhancing during that period,21 the ventricular volume at peak-ejection may be estimated by the formula: (RVEDV -2SV/3).
RAP represents the RV pressure at end-diastole (end-filling period).22
Pulmonary artery diastolic pressure (PADP) represents the RV pressure at end-isovolumic systole. The end-isovolumic systole point is on the point of pulmonic valve opening and the start of RV ejection, in other words it's on the point of the RV systolic pressure exceeding the level of the PAP which is located on the diastolic period at that time. Therefore, PADP can be used to represent the RV pressure of the end-isovolumic systolic point.
Right ventricular systolic pressure (RVSP) is just the pressure at peak-ejection. In this study, at each time point of data collection, the PAC was advanced in the case of the tip balloon deflation to position the RAP orifice into the right ventricle, and then RV systolic and diastolic pressure were measured via the RAP orifice. To make sure of the validity and consistency of RVP at different time points, the depth of two positions of the PAC should be recorded. One was the depth where the PAC was positioned correctly after anesthesia induction; the other was the depth where the RVP waveform appeared via the RAP orifice after advancing the PAC first. Movement of PAC at each time point was just based on the depth of these two positions.
Pressure of pulmonary artery dicrotic notch (PDN) represents the RV pressure at end-systole. The end-systolic point is the time point when the pulmonic valve closes as the RV pressure declines below the level of PAP. This closure produces a small notch (dicrotic notch, DN) on the downslope of the PAP waveform that separates RV systole and diastole. Therefore, pressure of DN (PDN) can be used to represent the RV pressure of the end-systolic point. DN can be identified in terms of its particular shape and its occurrence after the T wave on the ECG.22,23 Thereby, PDN may be estimated according to the pressure scale on the monitor.
Right ventricular diastolic pressure (RVDP) is just the pressure of the end-isovolumic diastole point; at which filling of RV doesn't yet begin, so RVDP is the lowest value in a cardiac cycle.
The RV pressure-volume loops were constructed automatically after putting the above pressure and volume data into the computer. Since the right ventricle has a complex structure and physiology,4 these pressure-volume loops constructed by this way were just simplified and schematic diagrams, not a real-time framework of RV performance.
Statistical analysis was performed using SPSS13.0. All data were presented as mean ± standard deviation (SD). One-way analysis of variances (ANOVA) was used to compare data within groups. Multiple comparisons were performed using LSD procedure. A P value <0.05 was considered statistically significant.
Patients and operative characteristics
There were 28 patients included according to the criteria of patient selection in this study. Patients’ characteristics were shown in Table 1. Coronary anastomoses were performed successfully in all patients and the average number of bypass vessels was 3.4±0.7 per patient. The total amount of fluid infusion was (2629.1±567.4) ml per patient. There was no significant change in the amount of fluids infused at different time points.
Changes of right ventricular hemodynamic variables
Changes in RV hemodynamic variables at different time points are shown in Table 2. RVEF at T4 decreased significantly (P <0.05) compared with values at T1. RVEDVI at T3, T4 and T5 decreased significantly (P <0.05) compared with values at T1. Changes in SVI resembled RVEDVI, but compared with both values at T1, the degree of decrease in SVI by 18% was greater than that in RVEDVI by 10% at T4. PVRI at T1 was higher than that at any other time points (P <0.05), but from T2 to T4, PVRI increased progressively and decreased again at T5. RAP increased significantly (P <0.05) during anastomoses (T2, T3, T4) compared with values at T1 and decreased again at T5. There were no significant changes in PAWP at different time points. MAP declined at T3 and T4.
Changes of right ventricular pressure-volume loops
In all patients, complete pressure-volume data were acquired at five time points during OPCAB surgery. RV pressure-volume loops in one representative patient are shown in Figure. The figure was constructed automatically by a computer with pressure-volume data measured from end-diastole point, end-isovolumic systole point, peak-ejection point, end-systole point and end-isovolumic diastole point using a volumetric PAC. The shape of RV pressure-volume loops were approximately triangular as first reported by Maughan and colleagues.24 Although the figure was simplified and schematic, they showed clearly that right ventricular P-V loops generally shifted to the left during OPCAB surgery. Meanwhile, emphasis was placed on the A point and A′ point that were just the end-diastolic point and end-systolic point. Compared with that at T1, A point shifted upward and to the left distinctly from T2 to T5. For A′ point, there was no distinct shift at T5 compared with that at T1 despite some changes during coronary anastomoses (T2, T3 and T4).
Changes of right ventricular EES and EED
Changes in EES and EED at different time points are shown in Table 3. The change of EES was not statistically significant during operation. Compared with values at T1, EED increased significantly from T2 to T4 (P <0.05). Although EED at T5 decreased to some extent, it didn't return to the level before operation (P<0.05).
Characteristics of anesthetic management
Dopamine was continuously administered prior to heart displacement, so the MAP was maintained ≥60 mmHg and norepinephrine was hardly used during coronary anastomoses. The proportion of patients administered dopamine at T3 and T4 was about 96% and the amount of dopamine at these two time points was also higher than that at other time points; which was (3.19±1.60) μg•kg−1•min−1 at T3 and (3.00±1.62) μg•kg−1•min−1 at T4.
ST-segment elevation or depression (>0.1 mv for over 60 seconds)20 was observed in five patients, which occurred at T3 and T4. These ST changes were stabilized with repositioning of the heart and adjusting the dosage of isosorbide dinitrate appropriately. Nevertheless, when the heart is completely displaced, the diagnostic accuracy of ECG monitoring is reduced.25 Arrhythmia occurred temporally with heart displacement and returned to the normal rhythm after the heart stabilized.
Our study demonstrated that right ventricular P-V loops can be constructed with the pressure and volume data measured using a volumetric PAC. The changes of P-V loops as well as EES and EED, indicated that RV diastolic dysfunction occurred significantly throughout OPCAB surgery, whereas there was no significant change in RV systolic function after sternal closure compared with that before operation.
Ventricular pressure-volume relationships have been shown to provide relative load-independent indices of cardiac function.10–15 New methodological aspects in this study include the way to construct right ventricular P-V loops with pressure and volume data at the end-diastole point, end-isovolumic systole point, peak-ejection point, end-systole point and end-isovolumic diastole point in the cardiac cycle. There were no technical difficulties and measurements were uncomplicated for these data. The volume data for the P-V loops as well as EES and EED were measured with the volumetric thermodilution PAC and VigilanceTM monitor. Since some variables (RVEDVI, RVESVI, RVEF, SVI, CI) displayed on the VigilanceTM monitor were average values measured in the past 6—9 minutes, 5 minutes after application of a stabilizer (about 10 minutes from heart positioning) was selected to record data in our study. Kwak et al3 reported that this time point might be corresponding closely both to the average cardiac status for each coronary anastomosis and to the average values displayed in the VigilanceTM monitor of measurements during the past 6—9 minutes.
From Figure, compared with the position at T1, the end-diastolic point (A point) shifted upward and to the left distinctly from T2 to T5 (increase in EDP while decrease in EDV), which roughly conformed to the alterations of ventricular diastolic dysfunction.26 In other words, shifts in end-diastolic point indicated that the right ventricular chamber stiffness increased and the passive relaxation properties (or compliance) was reduced throughout OPCAB surgery. For the end-systolic point (A′ point), there was no distinct shift at T5 compared with that at T1, which suggested that contractile state of RV did not change significantly before and after operation despite some changes during coronary anastomoses (T2, T3 and T4) which were probably induced by the dopamine infusion.
Consistent with previous studies,7 the current study indicated that greater dysfunction of RV than that of LV might occur because MAP decreased with a concomitant increase in RAP whereas PAWP did not change during coronary anastomoses. In this study, a significant decrease in RVEF occurred during anastomoses on the posterior wall. Nevertheless, what RVEF reflects is the global systolic function of the ventricle and it has several determinants, including myocardial contractility, preload and afterload. For myocardial contractility, EES did not change significantly during operation, which demonstrated that the decrease in RVEF at T4 probably was not attributable to the impaired myocardial contractility. For preload, RVEDVI and SVI at T4 were the lowest values and the degree of decrease in SVI (18%) was greater than that in RVEDVI (10%). For PVRI, it declined significantly during the operation compared with level before operation, which might be due to the application of isosorbide dinitrate throughout the operation. Yet, heart displacement and compression appears to have important effects on PVRI because it increased progressively from T2 to T4 and decreased again after cardiac manipulations were finished at T5. Since RVEF is most sensitive to the change in afterload, so any increase in PVRI is accompanied by a substantial decrease in RVEF.27 Thus, it was concluded that a decrease in RVEF during anastomosis on the posterior wall might be due to significant decreases in SVI and RVEDVI and a relative increase in PVRI. In other words, decrease in RVEF at T4 didn't represent the impaired contractile state of RV.
Actually, acute myocardial ischemia can lead to not only systolic but also diastolic dysfunction of the ventricle, and that diastolic dysfunction may be the first or the only symptom of ischemia.28 In this study, increases in EED indicated that the RV passive relaxation properties was impaired, which might result from myocardial ischemia or RV compression from direct surgical manipulations on the beating-heart since the RV has thinner walls and lower pressure. Thus, impairment of compliance caused the RV to relax insufficiently and reduced the amount of RV passive filling, which became one of the key determinants of the decrease in RVEDVI. In a word, these results implied that the impaired diastolic function of RV might play an essential role in the hemodynamic derangement during OPCAB surgery.2,29
Compared with traditional methods,5,23 the way that right ventricular P-V loops and EES and EED were acquired was simplified in this study. Nonetheless, as far as clinical practice is concerned, this way combines the pressure with the volume to monitor cardiac status, which is more reasonable compared with evaluating cardiac function based upon only a single pressure or volume data. Besides, analysis of RV pressure-volume loops should primarily focus on the changing trend; partly because these figures were not a real-time framework of RV performance, but schematic, simplified diagrams. In addition, some factors, including disease severity, preoperative medication, surgical manipulations of the beating-heart and a variety of physiologic and pathophysiologic reflexes may affect the results.
In conclusion, right ventricular P-V loops can be constructed with pressure and volume data measured from several specific time-points in the cardiac cycle by a volumetric PAC. The RV systolic function was impaired significantly during anastomosis on the heart's posterior wall, not due to reduced myocardial contractility but as a result of reduced SVI and RVEDVI and relative increase in PVRI, and recovered at the end of surgery. The RV diastolic dysfunction occurred significantly throughout OPCAB surgery. These results were consistent with that derived from RV pressure-volume loops.
We thank Dr. Daniel Bainbridge and Dr. Davy Cheng (Department of Anesthesia & Perioperative Medicine, University of Western Ontario, London, Ontario, Canada) for their help in the preparation of this article.
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