Epidural anesthesia and postoperative analgesia with ropivacaine and fentanyl in off-pump coronary artery bypass grafting: a randomized, controlled study

Coronary artery bypass grafting (CABG) is one of the most common cardiosurgical interventions. In many institutions, CABG is performed without cardiopulmonary bypass (CPB), a modification which is commonly referred to as off-pump coronary artery bypass grafting (OPCAB) [1‐4]. The off-pump technique enables coronary revascularization on the beating heart, thereby reducing the risk of complications associated with CPB. However, OPCAB can be accompanied by hemodynamic alterations, postoperative pain, and respiratory dysfunction, requiring thorough monitoring and perioperative care [3‐6].

In cardiosurgical patients, high thoracic epidural anesthesia (EA) with local anesthetics and opioids can provide effective analgesia and reduce the number of perioperative complications [6‐8]. However, the use of EA in coronary surgery is controversial, and it is still unclear whether EA influences lung fluid balance, cardiopulmonary function and clinical outcome in OPCAB. Thus, the method requires further evaluation and its potential benefits in coronary patients should be weighed against its risks [8, 9].

Patient-controlled epidural analgesia (PCEA) is an attractive technique for postoperative pain relief. However, in OPCAB the role of PCEA with administration of a ropivacaine/fentanyl mixture via a thoracic epidural catheter remains unsettled.

We hypothesized that after OPCAB, thoracic epidural analgesia with ropivacaine and fentanyl aiming at a visual analog scale (VAS) score < 30 mm will be associated with improved cardiopulmonary parameters in comparison with intravenously administered analgesia. If the hypothesis is confirmed, we expect that epidural administration of ropivacaine and fentanyl, including a patient-controlled mode, might reduce the duration of mechanical ventilation. Thus, the duration of mechanical ventilation and the changes in cardiopulmonary variables served as the primary and the secondary study end-points, respectively. Using these end-points, the aim of our study was to assess the influence of EA followed by postoperative PCEA with ropivacaine/fentanyl on cardiopulmonary function in the perioperative management of OPCAB patients.

As shown in Table 1, we found no significant differences among the groups concerning demographic data, including co-morbidities and preoperative ejection fraction. Three patients (one patient in each group) who became hemodynamically unstable during CABG were transferred to CPB and excluded from further analysis (Figure 2). One of these patients (belonging to the EI group) required re-operation and died because of postoperative bleeding from the aorta. All the other patients survived to Day 28 and were discharged from hospital. Duration of surgery, as well as of ICU and hospital stays, did not differ among the groups. The duration of mechanical ventilation was reduced by 32% in the PCEA group (P = 0.04) and tended to decrease in the EI group (P = 0.14) compared with the control group (Table 1).

Table 2 displays changes in hemodynamics. In the groups receiving EA, MAP decreased transiently by 10-15% during OPCAB (P < 0.05), but rose postoperatively without intergroup differences. After induction of anesthesia, all groups demonstrated reduced HR, CI, CFI, dPmax and GEF, and increased SVRI as compared to normal values. Perioperatively, HR, CI, and CFI rose in all groups whereas SVRI declined (P < 0.05). Compared to baseline, CVP increased significantly at the restraint of the heart and then decreased after OPCAB in all groups (P < 0.05). Global end-diastolic volume index did not change significantly. In the EI and the PCEA groups, dPmax increased postoperatively by 70-85% (P < 0.05). By contrast, in the control group GEF decreased by 10-15% during OPCAB, and EVLWI rose by 22% during the restraint of the heart (P < 0.05).

Table 3 demonstrates blood gases and biochemical variables. In all groups, pH declined intraoperatively and during 6 h postoperatively, but increased significantly at 24 h in the groups receiving epidural analgesia. In parallel, PaCO₂ decreased from intragroup baseline during 12-24 h in the EI group and during 18-24 h in the PCEA group but without differences with control group where PaCO₂ also reduced at 24 h. At 18 h, PaO₂/FiO₂ was higher in the PCEA group (P = 0.03 compared with controls). Plasma concentrations of lactate and glucose rose postoperatively in all groups; however, in the PCEA group lactate fell by 33% compared with the control group (P = 0.04) at 18 h. After OPCAB, plasma concentrations of cortisol and troponin T increased without intergroup differences.

The VAS scores were within 20 mm at rest and 30 mm during coughing in all groups without intergroup differences excluding 12 h when VAS score was significantly lower in the PCEA group as compared to controls (Table 4). The level of postoperative sedation did not differ among the groups.

Table 5 shows that during OPCAB, EA reduced the consumption of propofol by 15% and fentanyl by 50% (P < 0.05). The postoperative requirement of ropivacaine increased by 20% in the PCEA group as compared with the EI group (P = 0.03). In both EA groups, the requirement of nitroglycerin decreased by a 7-fold intraoperatively and by a 2.5-fold after OPCAB (P < 0.05). Intraoperative inotropes/vasopressors were administered more frequently in the EA groups as compared with the control group (43% vs. 13%, respectively; P = 0.02). Colloids also were given more frequently in the patients receiving EA (75% vs. 37%, P = 0.01). After OPCAB, the incidence of colloid administration was higher in the EI group compared with the other groups (P < 0.05). Intraoperative fluid balance increased by 21% in the EA groups (P < 0.05). There were no significant differences in blood loss, urine output, administration of crystalloids and adverse events (not shown). There were no complications related to EA.

The present study demonstrates that EA with ropivacaine/fentanyl causes a moderate decrease in arterial pressure and prevents reduction of GEF and lung fluid accumulation during OPCAB. The epidural administration of ropivacaine and fentanyl reduces the requirement of nitroglycerin and intravenous agents for anesthesia and analgesia, but requires more frequent perioperative therapy with colloids and inotropes/vasopressors. Postoperatively, EI provides adequate analgesia and improves left ventricle myocardial contractility. Moreover, EI combined with PCA is associated with mild hyperventilation, transient improvement of oxygenation and tissue perfusion and decreased duration of mechanical ventilation after OPCAB in comparison with the control group.

The postoperative improvement of lung function observed in the PCEA group was accompanied by reduced time to tracheal extubation, but the durations of ICU and hospital stays did not differ significantly. These results are in accordance with other studies of EA in coronary surgery and can be explained by a wide range of confounding factors that are able to influence the length of hospitalization [8, 10‐17]. However, according to Sharma et al., the use of epidural analgesia in obese patients can shorten the ICU stay after OPCAB [13]. This effect was explained by a reduced incidence of respiratory complications in this category of high-risk patients. Earlier hospital discharge after EA for CABG was also reported by de Vries et al. [18].

After induction of anesthesia, all the groups presented with myocardial dysfunction and systemic vasoconstriction, as judged by the occurrence of bradycardia, decreased CI, CFI and dPmax, and increased SVRI. The restraint of the heart was accompanied by a rise in CVP, paralleled by a decline in GEF and an increase in EVLW in the control group. This is typical for OPCAB and can be explained by "enucleation" of the heart, kinking of vessels, reduction of venous return, and impairment of ventricular geometry [1, 19]. After OPCAB, we observed a reduction of systemic vascular tone and a rise in myocardial performance. These changes are consistent with other investigations of CABG and may result from the restoration of coronary blood flow and reversal of myocardial depression by goal-directed hemodynamic optimization [1, 19, 20]. As shown in several previous studies, volumetric parameters measured by transpulmonary thermodilution, such as GEDVI, which we used for hemodynamic optimization, is a more sensitive indicator of preload compared to CVP and can serve as guidance for colloid administration [19‐24]. Most likely, this allowed us to maintain normal preload in all groups.

During OPCAB, EA decreased MAP transiently and partly prevented the decline in GEF as well as lung water accumulation, which we observed in the control group. In addition, in contrast to the control group, postoperative EI prompted a significant increase in dPmax. Although displaying only statistical intragroup differences, these changes can be explained by the hemodynamic effects of epidural blockade, including afterload reduction, that can lead to improvements in myocardial performance and pulmonary blood flow [7, 10, 25, 26]. Recently, similar findings were noticed by investigators, who used EA in on-pump CABG [25, 26].

The changes in hemodynamics observed during and after OPCAB were accompanied by transient metabolic acidosis and increased plasma lactate in parallel with hyperglycemia and rise in cortisol and troponin-T plasma concentrations in all groups. These data are consistent with results published by other authors and can be explained by tissue hypoperfusion, inflammation, surgical stress and myocardial damage caused by CABG [1, 14, 26, 27].

We found that epidural analgesia after OPCAB resulted in mild hyperventilation. Moreover, the PCEA with ropivacaine/fentanyl led to transient postoperative improvement in arterial oxygenation and decreased lactate, possibly due to improvement of pulmonary and systemic perfusion [28]. In addition to these mechanisms, the advantageous respiratory effects of epidural blockade in cardiac surgery were associated with reduced incidence of postoperative atelectases and improved quality of analgesia [15‐17, 28]. In our study, epidural anesthesia and analgesia provided adequate pain control, similar to that observed after administration of opioids in the control group, as confirmed by VAS score < 30 mm in both epidural groups; optimal analgesia was observed after PCEA. Thus, the combined effects of analgesia, pulmonary vasodilation, prevention of lung edema and improvement of pulmonary mechanics might have resulted in a better lung function in the PCEA group that allowed earlier termination of respiratory support.

In the present study, the analgesic effect of epidural administration of ropivacaine and fentanyl reduced the requirements of intravenously administered fentanyl and propofol for general anesthesia. The postoperative use of PCEA led to increased consumption of ropivacaine but did not influence the incidence of adverse events after OPCAB, like oversedation, pruritus, nausea, vomiting or arrhythmias. This is consistent with other investigations in this field. By contrast, several authors report reduced incidence of atrial fibrillation after EA for coronary surgery, probably due to the sympatholythic action of epidural blockade [11, 15, 28‐30]. Thus, by reducing the requirements in opioids, time to tracheal extubation and number of complications, EA can become part of a fast-track concept of cardiac anesthesia that is aimed to achieve cost-savings, and improve clinical outcome, as suggested by recent workers [31]. Despite several beneficial effects of EA, we found increased requirements for colloids and inotrope/vasopressor support to maintain targeted hemodynamic values. This led to increased intraoperative fluid balance that also might have influenced cardiopulmonary function. In parallel, thoracic epidural administration of ropivacaine and fentanyl resulted in significant reduction of perioperative nitroglycerin requirement. These changes can be explained by vasodilation and redistribution of blood volume caused by EA and analgesia. Thus the hypotensive effect of epidural blockade should not be underestimated, especially in hemodynamically unstable patients. Similar results were obtained by other authors studying EA in coronary surgery [10, 11, 28].

A limitation of this patient-controlled mode of analgesia is that its use depends on the condition of the patient. Moreover, some of the effects of PCEA on cardiopulmonary function occurred transiently and their clinical significances should be interpreted with caution. Therefore, larger studies are warranted to confirm our findings and to determine the optimal regimens of EA and postoperative analgesia in OPCAB patients.

The use of EA during OPCAB reduces transiently arterial pressure and prevents lung fluid accumulation. Being a component of a goal-directed perioperative strategy, the epidural administration of ropivacaine/fentanyl can improve myocardial performance and provide analgesia comparable with intravenous opioids, although increasing the requirements for fluids and vasoactive therapies. After OPCAB, continuous EI combined with PCEA increases tissue perfusion and improves lung function, thus shortening the duration of mechanical ventilation.