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Alteration of baroreflex control of heart rate after hepatectomy

Kavafyan, J.; Samain, E.; Marty, J.; Belghiti, J.

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European Journal of Anaesthesiology: March 2004 - Volume 21 - Issue 3 - p 249-251


The anaesthetic-induced depression of baroreflex control of heart rate is restored shortly after discontinuation of the anaesthetic [1]. This is of critical importance in the perioperative period as an intact baroreflex function is necessary to ensure haemodynamic stability [2]. Certain surgical procedures may also induce specific alteration of cardiovascular function, superimposed on the effect of anaesthesia. In this regard, hepatic surgery using portal triad clamping has been reported to induce a reflex activation of the nervous sympathetic system in response to a decreased venous return. However, its effect on baroreflex function in the postoperative period is unknown. The present prospective study tested the hypothesis that baroreflex control of heart rate could be depressed in the early postoperative period after hepatectomy with portal triad clamping.

After institutional approval, 14 patients scheduled for hepatectomy with intermittent portal triad clamping (20 min of clamping followed by 5 min of release) gave written informed consent to participate in the study. Exclusion criteria were: (a) a past medical history of hypertension, coronary artery disease, congestive heart failure and diabetes mellitus; (b) current treatment with β-adrenoceptor-blocking drugs or any centrally acting antihypertensive medication; and (c) abnormal electrocardiogram (ECG). Patients were also excluded if mechanical ventilation of the lungs lasted more than 24 h after the end of surgery. After premedication with hydroxyzine, invasive arterial pressure (radial artery) was recorded simultaneously with the ECG on a Gould recorder (model PX 1800®; Baxter Healthcare Corporation, Deerfield, IL, USA). After 30 min of rest (baseline: T1), baro-reflex control of heart rate was assessed using the pressor test method [3]. Briefly, an increase in systolic arterial pressure of 20-30 mmHg over 20-30 s was induced by intravenous injection of phenylephrine. The dose of phenylephrine was determined individually for each patient. The relationship between the systolic arterial pressure and the succeeding R-R interval (ms) on the ECG was determined during the increasing phase of systolic arterial pressure. Fifteen to 20 systolic arterial pressures and R-R intervals were plotted on a beat-to-beat analysis, and the slope of the relation-ship (expressed as ms mmHg−1), calculated by linear regression analysis, was used as an index of the baroreflex gain. Regression slopes with a correlation coefficient (r2) less than 0.7 were excluded. General anaesthesia was induced with thiopental and fentanyl, and pancuronium facilitated endotracheal intubation. The patients' lungs were mechanically ventilated and anaesthesia was maintained with nitrous oxide in oxygen (50/50%), isoflurane and fentanyl. Intraoperative hypothermia was prevented using an air-warming blanket. Patients were allowed to recover in the operating room or intensive care unit. A second set of baroreflex function assessment (postoperative: T2) was performed on the first postoperative day in the intensive care unit, at least 4 h after tracheal extubation, in clinically stable patients. Postoperative analgesia was provided with intravenous morphine (titration followed by patient-controlled analgesia: 1 mg bolus, 10 min refractory period).

Patient characteristics and haemodynamic data, or baroreflex gain, are expressed as mean ± SD, or median and interquartile, respectively. Haemodynamic data or baroreflex gain measured at T1 and T2 were compared using a t-test for paired values or the U-test, respectively, using Statview® 6.0 software (SAS Institute, Cary, NC, USA). P < 0.05 was considered as statistically significant.

One patient was excluded because of delayed endotracheal extubation, and another three because surgery could not be performed as planned. Ten patients were finally included in the analysis (six males/four females, aged 55 ± 14 yr, body mass index 25 ± 7 kg m−2, ASA I/II 7/3). Surgery lasted 5.5 ± 1.3 h, with a cumulative portal triad clamping duration of 44 ± 23 min. The mean duration of endotracheal intubation and the time between extubation and postoperative baroreflex assessment were 10.2 ± 6.7 and 13.0 ± 1.5 h, respectively. The mean systolic arterial pressure was not different at T1 (130 ± 27) and at T2 (112 ± 10 mmHg, P = 0.15), whereas heart rate was significantly higher at T2 (88 ± 14) compared with T1 (68 ± 11 beats min−1; P < 0.01). Baroreflex gain decreased in the postoperative period (T2: 3.6 ± 2.6 ms mmHg−1) compared with (T1: 10.0 ± 8.4 ms; P = 0.015) (Fig. 1), whereas the R-R interval calculated at reference systolic arterial pressure was unaltered (T1: 770 ± 256; T2: 736 ± 178 ms).

Figure 1
Figure 1:
Individual and median values of baroreflex gain measured before (preoperative) and after (postoperative) hepatic resection. *P < 0.05 postoperative versus preoperative.

The study demonstrated a decrease in baroreflex sensitivity after hepatectomy with intermittent portal triad clamping. These results differ from those obtained by Carter and colleagues, who demonstrated that baroreflex function was rapidly restored in the postoperative course in healthy patients even before complete recovery from anaesthesia [1]. In contrast, an alteration of the baroreflex control of heart rate of similar magnitude than observed was reported in hypertensive patients who underwent orthopaedic or abdominal non-hepatic surgery [4]. The present results strongly suggest that hepatic resection with portal triad clamping alters baroreflex gain. The mechanisms involved in this effect remain speculative, but may be related to the sustained stimulation of the sympathetic nervous system induced by hepatic surgery. In this regard, the stimulation of the coeliac plexus and splanchnic nerves during upper abdominal surgery depresses the arterial baroreflex [5]. Although the effect of portal triad clamping by itself cannot be assessed, since it is now commonly used to reduce blood loss during hepatectomy, portal triad clamping may have reinforced the intraoperative stimulation of the sympathetic nervous system. Portal triad clamping decreases hepatic and splanchnic blood flow and induces a moderate decrease in cardiac output [6]. These haemodynamic changes, along with the stimulation of pressor receptors located in the portal venous system induced by an increase in venous portal pressure, lead to an increase in sympathetic nervous system activation and systemic vascular resistance [7]. In contrast, the release of humoral mediators, e.g. vasopressin, suggested to occur after portal triad clamping is probably of minimal importance in acute haemodynamic variations observed after clamping and unclamping.

The clinical significance of the sustained decrease in baroreflex sensitivity deserves further investigation, and it can be speculated that the haemodynamic response to acute alteration in arterial pressure, which may occur for several reasons in the postoperative period, may be attenuated. In conclusion, the study showed that baroreflex control of heart rate is decreased in the early postoperative period in healthy patients undergoing hepatectomy with portal triad clamping. This effect may be related to intraoperative haemodynamic alterations induced by surgery. The results suggest that interpretation of haemodynamic variations postoperation should taken into account when studying alterations of baroreflex function.

J. Kavafyan

E. Samain

J. Marty

Department of Anaesthesiology and Intensive Care; Hôpital Beaujon; Clichy, France

J. Belghiti

Service de Chirurgie Digestive; Hôpital Beaujon; Clichy, France


This work was supported by a grant from the Délégation à la Recherche Clinique, Assistance Publique-Hôpitaux de Paris, 3 avenue Victoria, Paris, France.


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© 2004 European Society of Anaesthesiology