In gynaecological laparoscopies, the insufflation of carbon dioxide for the creation of a prolonged pneumoperitoneum as well as the adoption of the lithotomy position with steep head-down tilt have potential haemodynamic and respiratory consequences. The increased pressure within the abdomen influences the intrathoracic pressures by pushing the diaphragm upward, thus decreasing respiratory system compliance [1,2]. Branche et al.  demonstrated that intraperitoneal insufflation of carbon dioxide was associated with an increase in left ventricular afterload assessed by left ventricular end-systolic wall stress (LVESWS). Previous studies analysing haemodynamic changes induced by laparoscopic insufflation have reported enhanced mean arterial pressure (MAP) associated with an increase in systemic vascular resistance, with cardiac output (CO) being measured by noninvasive techniques [4–6], or even by thermodilution [7,8]. However, these and other cardiovascular variables usually return to preinsufflation values after a relatively short duration of pneumoperitoneum. Moreover, a lower intraabdominal pressure (IAP) (approximately less than 15 mmHg) is required, in so far as it reduces the risks associated with high pressures . For pelvic procedures, a higher IAP of approximately 25 mmHg is used, but during the abdominal procedures, IAP is not allowed to exceed 15 mmHg. Higher pressures are associated with faster CO2 absorption and gas embolism . Moreover, hypercarbia causes myocardial depression . These effects are further influenced by the intraoperative position of the patient and duration of procedure. To evaluate these haemodynamic changes, most investigators have used pulmonary artery catheterization or transoesophageal echocardiography, though they are not routinely used monitoring techniques. Diastole begins at the closure of the aortic valve and lasts until the closure of the mitral valve. Diastole can be divided into two phases: the first corresponds to the left ventricular pressure decline at a constant volume, isovolumetric relaxation, which lasts from closure of the aortic valve to opening of the mitral valve; the second, auxotonic relaxation, corresponds to left ventricular chamber filling and lasts until the closure of the mitral valve. Left ventricular filling mainly depends on the pressure gradient between the left atrium and left ventricle, which is mainly influenced by passive chamber properties (compliance), active relaxation and, at end-diastole, by atrial contraction. Thus, impairment of left ventricular compliance (decreased atrioventricular pressure gradient), or the loss of atrial contraction, directly impairs diastolic filling. Left ventricular diastolic dysfunction refers to abnormalities of diastolic distensibility, filling or relaxation, regardless of whether left ventricular ejection fraction is normal. Left ventricular diastolic dysfunction can be defined as the inability of the left ventricle chamber to fill up at low atrial pressures. This dysfunction can result either from an impairment in left ventricular compliance (passive mechanism) or from an alteration in left ventricular relaxation (active process). Diastolic function is determined by the passive elastic properties of the left ventricle and by the process of active relaxation. Analysis of the mitral inflow velocity by Doppler echocardiography is widely used for the noninvasive assessment of the left ventricular diastolic filling . If the Doppler window is placed at the tip of the mitral valve, the diastolic flow velocity profile will reflect the pressure gradient between the left atrium and the left ventricle . The mitral blood flow is composed of an E (early) wave for passive diastolic filling followed by an A (atrial) wave for atrial systole. The mitral blood flow profile is affected by left ventricular relaxation, compliance and left atrial pressure. Normal diastole is characterized by a predominant E-wave (peak and area under the curve), implying that most of the left ventricular filling is occurring during the early phase of diastole. When only relaxation is impaired and atrial contraction contributes relatively more to ventricular filling, the A-wave is taller than the E-wave with prolonged E deceleration time and prolonged isovolumetric relaxation time (IVRT). When relaxation is impaired, left ventricular compliance is decreased and atrial pressure increased, there is a predominant E-wave, and both deceleration and IVRTs are reduced. The study was designed to explore the hypothesis that an increase in afterload – during capnoperitoneum – induces a delay in the onset of relaxation while causing a prolongation of the E-wave deceleration time as well as of the IVRT.
After institutional ethics committee approval, we obtained the written, informed consent of 10 female patients scheduled for laparoscopic hysterectomy and of 10 female patients scheduled for conventional open hysterectomy (COH) for enrolment in this study. All patients were ASA physical status I and had no cardiac, renal or respiratory disease. The patients received oral premedication with midazolam (50 μg kg−1) 1 h before surgery. General anaesthesia was induced intravenously, after preoxygenation, with propofol (1.5–2 mg kg−1), fentanyl (1–2 μg kg−1) and vecuronium (0.1 mg kg−1). After tracheal intubation, general anaesthesia was maintained with nitrous oxide (50%) in oxygen and sevoflurane (1.5–2%, end-tidal concentration) and intermittent doses of fentanyl. The minute ventilation was adjusted to maintain end-tidal (etCO2) concentrations between 30 and 32 mmHg. The surgical technique was similar for all patients. The CO2 insufflation was performed with the patients placed in the supine position, and IAP was automatically maintained at 14–15 mmHg. Intraoperative monitoring included continuous electrocardiography (leads II and V5), pulse oximetry, MAP, peak airway pressures and etCO2 concentrations. Echocardiographic measurements were recorded preoperatively in the recovery room (T0); after the induction of anaesthesia in the supine-lithotomy position (T1); 15 min after the creation of pneumoperitoneum, when 15 mmHg of IAP was reached, for the laparoscopic hysterectomy group (T2); 15 min after turning the patients into the Trendelenburg position for the laparoscopic hysterectomy and COH groups (T3); when the operation was completed in the supine position (T4). All echocardiographic recordings were acquired by a single experienced physician with a multifrequency Doppler transducer placed at the cardiac apical window during normal respiration before and during mechanical ventilation thereafter, according to the guidelines of the American Society of Echocardiography . CO was calculated by multiplying the velocity–time integral (VTI) of the mitral inflow by the cross-sectional area of the mitral ostium (A) and the heart rate (HR): CO = VTI × A × HR. Mitral inflow was measured using pulsed-wave Doppler positioned between the tips of mitral valve leaflets. Peak values of the E-wave and A-wave, VTIs of the E-wave and A-wave and deceleration time of the E-wave were registered. IVRT was measured using continuous-wave Doppler. Abnormal left ventricular relaxation and filling were classified according to the European Study Group on Diastolic Heart Failure . Left ventricular relaxation was regarded as slow if IVRT was more than 100 ms. Early left ventricular filling was regarded as slow if the ratio of the peak values of the E-wave and A-wave was less than 1 or deceleration time more than 220 ms.
Data were analysed using the statistical package SPSS 15.0 version (SPSS, Inc., Chicago, Illinois, USA). Continuous variables are expressed as mean ± SD, categorical variables are displayed as frequencies. The appropriate nonparametric statistical test was used to analyse intragroup or intergroup comparisons [Mann–Whitney U-test, Wilcoxon test or Friedman analysis of variation (ANOVA)]. A two-tailed P value less than 0.05 was considered significant.
Patients' characteristics and details of the operation are shown in Table 1. The two groups were comparable with respect to age and BMI. In Table 2, haemodynamic and echocardiographic data are shown. At T0, we performed echocardiography in awake patients, and measurements represent baseline values for the whole study population. After induction of anaesthesia (T1), we observed a small decrease in HR and MAP, yet no changes in the echocardiographic parameters were detected in either group. In the laparoscopic group, CO2 insufflation increased MAP and HR [from 75.9 ± 7.4 mmHg to 96.3 ± 14.2 mmHg and from 69 ± 5 beats per minute (bpm) to 76 ± 4 bpm, respectively] and produced a nonsignificant drop in CO, from 4.7 ± 0.5 to 4.1 ± 0.4 l min−1. Furthermore, we observed a significant decrease in stroke volume (SV) from 71.6 ± 7.0 to 65.3 ± 5.5 ml (P < 0.05) and left ventricular end-diastolic volume (LVEDV) from 108.9 ± 6.3 to 102.8 ± 5.5 ml (P < 0.05). At same time (T2) deceleration time and IVRT were prolonged from 178.7 ± 7.2 to 188.8 ± 8.3 ms and from 81.0 ± 4.7 to 111.6 ± 4.2 ms, respectively (Figs 1 and 2, Table 2), and both the E and A-wave velocities were diminished (Fig. 3), without any significant modification of the E/A ratio (Table 2).
In the conventional hysterectomy group, head-down tilt (T3) did not affect the diastolic parameters, but CO, SV and LVEDV increased (Table 2). Trendelenburg positioning led to the same changes also in the laparoscopic group, with a return to presurgery values.
At the end of surgery, once the table was returned to the horizontal position (T4), all haemodynamic variables and echocardiographic parameters registered did not differ from baseline values in either the laparoscopic hysterectomy or COH groups.
Through the combined use of transthoracic echocardiography and noninvasive haemodynamic monitoring, our investigation provided an evaluation of the cardiovascular responses, which occurred during hysterectomy in a population of young healthy women. For all patients enrolled, left ventricular systolic function, as expressed by the ejection fraction (Table 2), was preserved during all phases of the surgery. Authors described that after capnoinsufflation, there is an increase in total systemic vascular resistances and MAP [8,16,17]. Our study confirmed that in patients with normal left ventricular dimensions, peritoneal insufflation was associated with an increase in MAP (i.e. augmented afterload). In healthy patients, Joris et al. observed a 30–40% reduction in cardiac index after capnoinsufflation, by using the thermodilution technique. In the study conducted by Larsen et al. , the left ventricular end-diastolic and end-systolic diameters were significantly increased in the presence of carbon dioxide pneumoperitoneum, reflecting an increased venous return irrespective of position. Zuckerman et al. observed a significant reduction in LVEDV during carbon dioxide pneumoperitoneum but no further changes when the patient was placed in the reverse Trendelenburg position. In our patients, we found that pneumoperitoneum led to a reduction in LVEDV. We measured LVEDV as an index of volume status. This variable decreased after CO2 insufflation and increased up to baseline values after Trendelenburg positioning, probably due to the pool in the lower extremities and thus a reduction in venous return induced by capnoinsufflation and reversed by head-down tilt. Furthermore, we found a nonsignificant drop in CO yet a considerable reduction in SV. We thought that the decrease in SV caused by pneumoperitoneum had been compensated by the rise in HR, so the CO had no significant variations.
Undoubtedly, in this context, carbon dioxide pneumoperitoneum is not the only influence on the cardiovascular system. Another major influence is posture. Head-down tilt with pneumoperitoneum causes a return of the afterload to basal values, while increasing the preload.
In this work, we have focused on diastolic function. To our knowledge, no data about the relationship between pneumoperitoneum and left ventricular filling times appear in the literature. In our study, we observed that CO2 insufflation prolonged both the E-wave deceleration and IVRTs. Furthermore, Trendelenburg positioning did not modify IVRT yet produced a further prolongation of deceleration time. Conversely, during head-down tilt in laparotomic hysterectomy, deceleration time registered the same increase as in laparoscopy, but IVRT remained stable. The E/A ratio showed no significant variations during the whole study in either laparoscopic hysterectomy or COH, but the waves were singularly influenced by pneumoperitoneum and Trendelenburg positioning; indeed, capnoinsufflation reduced both E and A-wave velocities in the laparoscopic hysterectomy group, and during Trendelenburg positioning, the E-wave further decreased while the A-wave rose; in the COH group, head-down tilt caused the same variations.
These results suggest that the augmented afterload induced by capnoperitoneum modifies the left ventricular filling times, producing an impairment of the early phase of diastole, as shown by E-wave velocity reduction and IVRT and deceleration time prolongation; afterwards, the augmented preload caused by Trendelenburg positioning induces a further E-wave velocity reduction and deceleration time prolongation.
During augmented afterload, the heart needs more time to fill, preventing an increase in intracavitary pressures.
The authors thank Liliana Inglese for her helpful assistance with the language revision.
1 Odeberg S, Ljungqvist O, Svenberg T, et al
. Haemodynamic effects of pneumoperitoneum
and the influence of posture during anaesthesia for laparoscopic surgery. Acta Anaesthesiol Scand 1994; 38:276–283.
2 Hirvonen EA, Nuutinen LS, Kauko M. Haemodynamic due to Trendelenburg positioning and pneumoperitoneum
during laparoscopic hysterectomy. Acta Anaesthesiol Scand 1995; 39:949–955.
3 Branche PE, Duperret SL, Sagnard PE, et al
. Left ventricular loading modifications induced by pneumoperitoneum
: a time course echocardiography study. Anesth Analg 1998; 86:482–487.
4 Critchley L, Critchley J, Gin T. Hemodynamic changes in patients undergoing laparoscopic cholecystectomy: measurement by transthoracic electrical bioimpedance. Br J Anaesth 1993; 70:681–683.
5 Westerband A, Van De Water J, Amzallag M, et al
. Cardiovascular changes during laparoscopic cholecystecotmy. Surg Gynecol Obstet 1992; 175:535–538.
6 Girardis M, Broi U, Antonutto G, Pasetto A. The effect of laparoscopic cholecystectomy on cardiovascular function and pulmonary gas exchange. Anesth Analg 1996; 83:134–140.
7 Gannedahl P, Odeberg S, Brodin L, Sollevi A. Effects of posture and pneumoperitoneum
during anaesthesia on the indices of left ventricular filling. Acta Anaesthesiol Scand 1996; 40:160–166.
8 Harris S, Ballantyne G, Luther M, Perrino A. Alterations of cardiovascular performance during laparoscopic colectomy: a combined hemodynamic and echocardiographic analysis. Anesth Analg 1996; 83:482–487.
9 Wolf JS Jr, Stoller ML. The physiology of laparoscopy: basic principles, complications and other considerations. J Urol 1994; 152:294–302.
10 Cooperman AM. Complications of laparoscopic surgery. In Aregui ME, Fitzgibbons RJ, Katkhouda N, et al.
, editors. Principles of laparoscopic surgery: basic and advanced techniques
. New York: Springer-Verlag, 1995; pp. 72–77.
11 Rasmussen JP, Dauchot PJ, DePalma RG, et al
. Cardiac function and hypercarbia. Arch Surg 1978; 113:1196–1200.
12 Ommen SR, Nishimura RA, Appleton CP, et al
. Clinical utility of Doppler echocardiography and tissue Doppler imaging in the estimation of left ventricular filling pressure: a comparative simultaneous Doppler-catheterization study. Circulation 2000; 102:1788–1794.
13 Appleton CP, Hatle LK, Popp RL. Relation of transmitral flow velocity patterns to left ventricular diastolic function
: new insights from a combined hemodynamic and Doppler echocardiographics study. J Am Coll Cardiol 1988; 12:426–440.
14 Lang RM, Bierig M, Devereux RB, et al
. Recommendations for chamber quantification: a report from the American Society of Echocardiography's Guidelines and Standard Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr 2005; 18:1440–1463.
15 European Study Group on Diastolic Heart Failure. How to diagnose diastolic heart failure. Eur Heart J
16 O'Malley C, Cunningham AJ. Physiologic changes during laparoscopy. Anesthesiol Clin North Am 2001; 19:1–19.
17 Joris JL, Noirot DP, Legrand MJ, et al
. Hemodynamic changes during laparoscopic cholecystectomy. Anesth Analg 1993; 76:1067–1071.
18 Larsen JF, Svendsen FM, Pedersen V. Randomized clinical trial of the effect of pneumoperitoneum
on cardiac function and haemodynamics during laparoscopic cholecystectomy. Br J Surg 2004; 91:848–854.
19 Zuckerman R, Gold M, Jenkins P, et al
. The effects of pneumoperitoneum
and patient position on hemodynamics during laparoscopic cholecystectomy. Surg Endosc 2001; 15:562–565.