Left ventricular regional wall motion abnormalities during pneumoperitoneum in children

E. Huettemann1, S. G. Sakka1, G. Petrat1, F. Schier2 and K. Reinhart1

1 Department of Anaesthesiology and Intensive Care Medicine and 2 Department of Paediatric Surgery, Friedrich-Schiller-University Jena, Bachstrasse 18, D-07740 Jena, Germany

Corresponding author. E-mail: Egbert.Huettemann@med.uni-jena.de

Accepted for publication: February 14, 2003


    Abstract
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
Background. In adult patients, certain levels of PEEP (16 and 20 cm H2O) have been associated with left ventricular (LV) regional wall motion abnormalities. Since any increase in intra-abdominal pressure (IAP) exerted by a pneumoperitoneum is transmitted to the intrathoracic cavity, similar effects on LV regional wall motion cannot be ruled out.

Methods. To investigate the effects of pneumoperitoneum on LV regional wall motion, we performed a post hoc analysis of a transoesophageal echocardiography study in eight small children (mean age 3 yr, range 15–63 months) undergoing laparoscopic herniorrhaphy under anaesthesia with sevoflurane in nitrous oxide/oxygen and a PEEP of 5 cm H2O. During carbon dioxide insufflation, end-tidal carbon dioxide concentration was kept constant by increasing minute volume.

Results. An IAP of 12 mm Hg caused significant septal hypokinesia compared with baseline, while anterior and posterior wall motion was not affected. In addition, a lateral hyperkinesia occurred, though this change was not statistically significant.

Conclusions. Pneumoperitoneum may affect LV regional wall motion in paediatric patients undergoing laparoscopic surgery.

Br J Anaesth 2003; 90: 733–6

Key words: complications, pneumoperitoneum; heart, ventricles; surgery, laparoscopy


    Introduction
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
As in adults, laparoscopic techniques have become standard procedures in paediatric surgery.1 In adult patients, PEEP has been shown to affect left ventricular (LV) regional wall motion. In studies investigating the effects of PEEP on LV function in critically ill patients, PEEP levels of 16 and 20 cm H2O produced significant impairment of septal wall motion.2 3 Since the increase in intra-abdominal pressure (IAP) exerted by pneumoperitoneum is transmitted to the intrathoracic cavity, similar effects on LV regional wall motion cannot be ruled out. To our knowledge, no data exist on paediatric patients, and in particular, whether pneumoperitoneum affects LV regional wall motion. To study the effect of pneumoperitoneum on LV regional wall motion under general anaesthesia, we performed a post hoc analysis of a transoesophageal echocardiography (TOE) study in eight small children (mean age 3 yr, range 15–63 months) undergoing laparoscopic herniorrhaphy.4


    Patients and methods
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
After obtaining approval from the institutional ethics committee and informed parental consent, eight ASA I children (five male, three female; mean age 3.5 yr (range 2–6 yr); weight 17 (SD 4) kg) undergoing laparoscopic herniorrhaphy were studied. None of the children had cardiovascular, respiratory or cerebrovascular disease or was receiving medication.

All children received a standardized anaesthetic. After premedication with oral midazolam 0.5 mg kg–1, anaesthesia was induced with thiopental 5 mg kg–1 and fentanyl 0.005 mg kg–1, and maintained with sevoflurane 0.75 MAC and nitrous oxide 67% in oxygen.5 Intubation of the trachea was facilitated with rocuronium 0.6 mg kg–1. Surgery was performed in the supine position. All children underwent mechanical ventilation using a pressure-controlled mode (AS3, Datex-Engstrom, Finland). In all patients, the inspiratory:expiratory (I:E) ratio was 1:1 and end-expiratory pressure was maintained at 5 cm H2O throughout the procedure. To avoid haemodynamic changes induced by hypercapnia, end-tidal carbon dioxide tension (PE'CO2) was maintained constant throughout the study at 4.5 kPa. After abdominal insufflation, ventilatory frequency was increased from 15 to 20 bpm and plateau inspiratory pressure was adjusted during the following three phases of pneumoperitoneum to maintain constant PE'CO2. After deflation of the abdomen, ventilatory frequency was reduced to pre-insufflation levels.

Non-invasive systolic, diastolic and mean arterial pressure, measured on the arm by oscillometry, heart rate (HR), peripheral oxygen saturation (SpO2), FIO2, PE'CO2, body temperature, respiratory minute volume, airway pressures, and inspiratory and end-tidal concentrations of nitrous oxide and sevoflurane were monitored throughout the study (AS 3, Datex, Helsinki, Finland). As the I:E ratio was 1:1, mean airway pressure (Pmean) was calculated as Pmean=PEEP+ inspiratory plateau pressure/2.

TOE was performed using a commercially available 7-mm monoplane 5.0-MHz paediatric probe (Agilent, Andover, MA, USA) which was connected to a Agilent Sonos 1000. All echocardiographic measurements were stored on video tape and analysed later by two independent investigators (EH, SGS). Echocardiography included a transgastric short-axis view at the midpapillary level for analysis of LV end-systolic and end-diastolic diameters and areas (expressed in terms of body surface area: end-systolic (ESAI) and end-diastolic (EDAI) area index), and for calculation of fractional shortening and fractional area change. Cardiac output (CO) was calculated by the velocity time integral (VTI) of the pulmonary artery Doppler flow profile, its diameter (d) and HR: CO=VTIx(d/2)2xHR. To account for respiratory changes in pulmonary artery flow profiles, consecutive heart beats in three respiratory cycles were analysed and averaged. The data regarding LV systolic function and systemic haemodynamics (CO, systolic wall stress, systemic vascular resistance) have been published.4 End-expiratory stop-motion frames at end diastole (peak of the R wave on simultaneous echocardiographic recording) and end systole (smallest ventricular dimension during the last half of the T wave) were displayed on a microcomputer screen to digitize the endocardial outlines of the left ventricle. Regional wall function was assessed using the centreline method described by Sheehan and colleagues,6 which is usually applied to contrast ventriculography. Regional wall motion was measured by the computer along 36 chords (c) constructed perpendicular to a centreline drawn midway between the end-diastolic and end-systolic contours on the short-axis view, and expressed in terms of absolute displacement during systole normalized for diastolic dimension.6 With this method, performed clockwise on a short-axis view of the left ventricle obtained by a transgastric approach, c 320–40° approximately involve the posterior wall, c 50–130° the lateral wall, c 140–220° the anterior wall, and c 230–310° the interventricular septum.

Study procedure
After stabilization of respiratory and haemodynamic variables, defined as changes in mean arterial pressure, HR, PE'CO2and expiratory anaesthetic gas concentrations of less than 10% within the previous 10 min, the first haemodynamic measurements were obtained (baseline). Carbon dioxide was then introduced to give an IAP of 12 mm Hg and haemodynamic measurements were repeated 10 min later. The IAP was then reduced to 6 mm Hg. After a 10 min period of 6 mm Hg, IAP was increased again to 12 mm Hg for 10 min (data not shown). The last haemodynamic measurements were obtained 10 min after abdominal deflation at the end of surgery, with the anaesthetic technique unchanged (control).

Data analysis
All values are expressed as mean (SD). Echocardiographic data obtained by two investigators were averaged. Statistical analysis was performed using ANOVA for repeated measurements and a pairwise multiple comparison procedure (Student–Newman–Keuls method, SigmaStat). A probability of less than 0.05 was considered statistically significant.


    Results
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
Haemodynamic and echocardiographic data are summarized in Table 1. The effects of pneumoperitoneum on regional wall motion are shown in Figure 1. In respect of the haemodynamic effects of pneumoperitoneum, an IAP of 12 mm Hg caused an increase in arterial pressure, systemic vascular resistance index, systolic wall stress, ESAI, EDAI and Pmean, and a decrease in HR and cardiac index (P<0.05) compared with baseline. Regarding regional wall motion, carbon dioxide insufflation into the abdominal cavity caused a reduction in septal (c 250–310°) wall motion (P<0.05) compared with baseline (Fig. 1). The lateral wall showed hyperkinesia without reaching statistical significance. After decreasing IAP to 6 mm Hg, cardiac index returned to baseline and there were no significant changes in regional wall motion. The second increase in IAP to 12 mm Hg led again to a reduction in septal wall motion. Fractional shortening was significantly lower than baseline at an IAP of 6 mm Hg and 12 mm Hg (Table 1). Fractional area change did not vary significantly under the various conditions.


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Table 1 Haemodynamic and respiratory changes. *P<0.05 compared with baseline; {dagger}P<0.05 compared with IAP 12 mm Hg; {ddagger}P<0.05 compared with IAP 6 mm Hg. (ANOVA for repeated measurements and a pairwise multiple comparison procedure (Student–Newman–Keuls method)
 


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Fig 1 Absolute value (mean) of left ventricular regional wall normalized motion measured along 36 chords (c) by the centreline method. A significant reduction in septal wall motion (c 250–310°) compared with baseline is observed with an intra-abdominal pressure of 12 mm Hg.*P<0.05. P=posterior wall, L=lateral wall, A=anterior wall, S=septal wall. Control represents values after deflation.

 

    Discussion
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
The main finding of this study is that an IAP of 12 mm Hg in small children may lead to regional wall motion abnormalities similar to those found in adults subjected to higher levels of PEEP. An IAP of 12 mm Hg caused septal hypokinesia while anterior and posterior wall motion was not affected. In addition, a lateral hyperkinesia occurred, though this change was not statistically significant.

In adults, PEEP has been shown to affect LV regional wall motion. In a study investigating the effects of PEEP on LV function in critically ill patients, a PEEP of 20 cm H2O produced significant impairment in septal kinetics.3 In another investigation in mechanically ventilated patients with acute respiratory failure, application of PEEP of 16 cm H2O resulted in a marked reduction in systolic septal wall motion and hyperkinesia of the lateral wall.2 An explanation postulated for these findings is a non-uniform transmission of the increased intrathoracic pressure to the LV wall because of its proximity to the pleural space.3 The mechanism by which pneumoperitoneum induces regional wall motion abnormalities is most likely similar to that of PEEP. Pneumoperitoneum also causes an increase in intrathoracic pressure but the degree of pressure transmission to the thoracic compartment varies. In animal studies, 30–40% of the IAP was transmitted to the thoracic cavity.7 8 Given an IAP of 12 mm Hg in our study, a similar degree of pressure transmission would have resulted in a rise in intrathoracic pressure of about 4 mm Hg (6 cm H2O). In studies in adults, PEEP levels of 10, 16 and 20 cm H2O led to increases in intrathoracic pressure (assessed by trans oesophageal pressure measurement [oesophageal balloon]), of 3.3, 5.5 and 5.6 mm Hg, respectively.2 3 Since it has not yet been investigated whether increased intrathoracic pressure from PEEP is comparable to a pressure generated from cephalad displacement of the diaphragm, it remains speculative whether the proposed mechanism for regional wall motion abnormalities induced by PEEP applies to pneumoperitoneum. In our study, we also applied a PEEP of 5 cm H2O which may not be common in clinical practice. However, we wished to prevent alveolar collapse from increased IAP, as has been suggested by Pighin and colleagues,9 who emphasized that functional residual capacity is less in small children and hypoxaemia may develop faster. In respect of the septal hypokinesia observed at an IAP of 12 mm Hg in our study, it remains uncertain whether the PEEP of 5 cm H2O contributed to the changes in wall motion, and if so to what extent. In respect of the effect of PEEP on lateral wall motion, one study in adults found significant changes in wall motion,2 while another did not.3 In this investigation, the hyperkinesia of the lateral wall during an increase in IAP to 12 mm Hg did not reach statistical significance. The PEEP levels used in adults (16 and 20 cm H2O) probably had a greater effect on intrathoracic pressure than that which resulted from the IAP of 12 mm Hg in our study. Furthermore, our patients exhibited a decrease in (global) fractional shortening with an IAP of 12 mm Hg. While this potentiated the decrease in septal wall motion, it reduced the increase in lateral wall motion.

When comparing our results with those investigating the effect of PEEP on LV regional wall motion, a major difference in the studies has to be noted. Creation of pneumoperitoneum leads to a significant increase of afterload, as shown by the increase in systemic vascular resistance index and systolic wall stress (a more reliable index of LV afterload) in our study (Table 1). In contrast, application of PEEP is associated with a decrease in afterload, thereby improving cardiac function and causing a reduction in LV size (diameter or end-diastolic area).3 In pneumoperitoneum, LV dimensions are influenced by two opposing effects: first, an increase in afterload resulting in a decrease in shortening fraction and fractional area change, and a concomitant increase in LV end-diastolic dimensions; and second, an increase in intrathoracic pressure. The increase in afterload explains why we found an increase, not a decrease, in LV dimensions during pneumoperitoneum, in contrast to studies on the effects of PEEP.

In this study, ventilation was adjusted in order to maintain PCO2 at a constant level. This approach avoided confounding results in respect of changes in CO caused by hypercarbia. However, an interaction between these changes in ventilation settings (increase in ventilatory frequency) and intrathoracic pressure, eventually influencing regional wall motion, cannot be ruled out. Since the adjustment of ventilation did not comprise changes in the I:E ratio and the tidal volume, it is unlikely that this change significantly influenced the results of our study. Besides its post hoc nature, our study is also limited by the fact that the intrathoracic pressure was not measured directly and that, for clinical reasons, we applied a PEEP of 5 cm H2O.

In conclusion, pneumoperitoneum may be associated with an inhomogeneity of regional LV systolic wall motion in small children. This may be the result of non-uniform transmission of the increased intrathoracic pressure to the LV wall because of its proximity to the pleural space. Whether changes in myocardial perfusion contribute to this phenomenon remains uncertain. This phenomenon may also be influenced by other factors such as lung compliance, ventricular function and filling status. These findings may render the evaluation of new regional wall motion abnormalities during pneumoperitoneum more difficult.


    References
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
1 Schier F, Montupet P, Esposito C. Laparoscopic inguinal herniorrhaphy in children: a three-center experience with 933 repairs. J Pediatr Surg 2002; 37: 395–97[CrossRef][ISI][Medline]

2 Schuster S, Weilemann SL, Erbel R, Meyer J. Inhomogeneity of left ventricular function during ventilation with positive endexpiratory pressure. Intensivmed 1998; 35: 114–23[CrossRef]

3 Fellahi JL, Valtier B, Beauchet A, Bourdarias JP, Jardin F. Does positive end-expiratory pressure ventilation improve left ventricular function? A comparative study by transesophageal echocardiography in cardiac and noncardiac patients. Chest 1998; 114: 556–62[Abstract/Free Full Text]

4 Sakka SG, Huettemann E, Petrat G, Meier-Hellmann A, Schier F, Reinhart K. Transoesophageal echocardiographic assessment of haemodynamic changes during laparoscopic herniorrhaphy in small children. Br J Anaesth 2000; 84: 330–4[Abstract]

5 Sarner JB, Levine M, Davis PJ, Lerman J, Cook DR, Motoyama EK. Clinical characteristics of sevoflurane in children. A comparison with halothane. Anesthesiology 1995; 82: 38–46[CrossRef][ISI][Medline]

6 Sheehan FH, Bolson EL, Dodge HT, Mathey DG, Schofer J, Woo HW. Advantages and applications of the centerline method for characterizing regional ventricular function. Circulation 1986; 74: 293–305[Abstract]

7 Marathe US, Lilly RE, Silvestry SC, et al. Alterations in haemodynamics and left ventricular contractility during carbon dioxide pneumoperitoneum. Surg Endosc 1996; 10: 974–8[CrossRef][ISI][Medline]

8 Rosenthal RJ, Friedman RL, Chidambaram A, et al. Effects of hyperventilation and hypoventilation on PaCO2 and intracranial pressure during acute elevations of intraabdominal pressure with CO2 pneumoperitoneum: large animal observations. J Am Coll Surg 1998; 187: 32–8[CrossRef][ISI][Medline]

9 Pighin G, Crozier TA, Weyland W, Ludtke FE, Kettler D. Specifics of anesthesiology in laparoscopic surgery in infancy. Zentralbl Chir 1993; 118: 628–30[ISI][Medline]