# Physiologic Responses to Infrarenal Aortic Cross-Clamping during Laparoscopic or Conventional Vascular Surgery in Experimental Animal Model: Comparative Study

Authors: María F. Martín-Cancho; Verónica Crisóstomo; Federico Soria; Carmen Calles; Francisco M. Sánchez-Margallo; Idoia Díaz-Güemes; Jesús Usón-Gargallo
Journal: Anesthesiology Research and Practice
 (2008)

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## Abstract

The aim of this study was to compare the hemodynamic and ventilatory effects of prolonged infrarenal aortic cross-clamping in pigs undergoing either laparotomy or laparoscopy.
18 pigs were used for this study.
Infrarenal aortic crossclamping was performed for 60 minutes in groups
I (laparotomy,n=6) and II (laparoscopy, n=6). Group III (laparoscopy, n=6) underwent a 120-minute long pneumoperitoneum in absence of aortic clamping (sham group).
Ventilatory and hemodynamic parameters and renal function were serially determined in all groups.
A significant decrease in pH and significant increase in PaCO2 were observed in group II, whereas no changes in these parameters were seen in group I and III. All variables returned to values similar to baseline in groups I and II 60 minutes after declamping. A significant increase in renal resistive index was evidenced during laparoscopy, with significantly higher values seen in Group II.
Thus a synergic effect of pneumoperitoneum and aortic cross-clamping was seen in this study. These two factors together cause decreased renal perfusion and acidosis, thus negatively affecting the patient's general state during this type of surgery.


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## Body

## 1. Introduction

Abdominal aortic surgery has improved greatly during the last 50 years, mainly thanks to advances in both anesthetic and surgical techniques. Abdominal laparoscopy is normally perceived to be associated with fewer risks [1]. However, clinicians should be aware of inherent dangers such as gaseous embolization, a potential inability to control hemorrhage, an increase in carbon dioxide arterial partial pressure, and changes in arterial blood pressure and heart rate. The hemodynamic and
respiratory alterations associated with abdominal laparoscopy are caused by the
high intra-abdominal pressure brought over by pneumoperitoneum creation. The
most relevant hemodynamic changes are a decrease in venous return secondary to
IVC compression and increases in central venous pressure and arterial blood
pressure in absence of heart rate changes. Regarding respiratory adjustments,
cranial displacement of the diaphragm causes a restrictive respiratory syndrome
with decreased pulmonary compliance and increased pulmonary pressures and
inspiratory peak [2, 3].When used in the management of aortic diseases, the laparoscopic approach poses further complications and risks that must be addressed, such as the long aortic
cross-clamping and surgical times [4]. Moreover, aortic cross-clamping in itself causes certain hemodynamic changes, whose effects must be taken into account along with the alterations secondary to laparoscopy. Previous human studies [4] reported severe
problems during aortic declamping and very prolonged anesthetic recovery times.Despite recent reports describing the feasibility of the
laparoscopic approach for the management of aortic occlusive and aneurismatic
disease [5–8] these studies focused
on the surgical technique and its technical feasibility, without assessing
hemodynamic and ventilatory stability or the patient’s recovery from the
procedure.Data compiled in a review written by Gelman in 1995 [9] demonstrated that aortic cross-clamping and declamping are associated to severe disturbances in homeostasis in
virtually all body systems. In experimental and clinical settings,
cardiovascular responses to aortic cross-clamping are characterized by
increases in proximal arterial pressure and systemic vascular resistance, while
cardiac output decreases [9–12].Prior studies by Byrne et al. [13] assessed physiological responses to laparoscopic aortobifemoral bypass surgery,
while Alfonsi et al. [14] focused their works on the evaluation of cardiac function during intraperitoneal CO2 insufflation for aortic surgery. However, those studies did
not evaluate the combination of the effects of aortic cross-clamping and
pneumoperitoneum during aortic surgery. Moreover, the anesthetic protocol used
in Byrne’s study [13] is no longer in clinical use in hospitals nowadays.We have found no studies evaluating pathophysiologic changes secondary to cross-clamping and declamping of the abdominal aorta during vascular laparoscopic surgery. With this in mind, we consider that the evaluation of physiologic changes occurring during infrarenal aortic surgery, whether using conventional surgery or laparoscopic techniques, is extremely important in order to determine whether the observed
hemodynamic changes can be attributed to pneumoperitoneum or aortic cross-clamping
alone or to the combined effect of these two factors. Understanding these
alterations will enable clinicians to improve the quality of anesthesia when
performing this kind of surgery. In our opinion, laparoscopic aortic
cross-clamping may cause physiological changes precluding the safe use of this
technique in all patients.


## 2. Materials and Methods

### 2.1. Animals

The experimental protocol was approved by the Institutional Ethical Committee for Animal Research. Eighteen healthy female large white pigs were used. Mean weight was30.8±2.0 kg.


### 2.2. Anesthesia

One day prior to the experimental anesthetic episode,
each pig was anesthetized with sevoflurane (Sevorane, Abbott Laboratories,
Madrid, Spain), and a 20-standard wire gauge catheter was placed in the carotid
artery and fixed to the skin. Similarly, on that same day a 4Fr. vascular
sheath was placed in the external jugular vein using the Seldinger technique.
Pigs were randomly assigned to 3 groups. Groups I(n=6) and II (n=6) underwent
aortic cross-clamping through either laparotomy in Group I or laparoscopy in
Group II. Animals belonging to Group III underwent a 120-minute long
laparoscopy in absence of aortic intervention (sham group). Food, but not water, was withheld for 8 hours
prior to surgery. Body temperature was maintained stable at 37-38ºC, using a
thermal blanket (Astopad system, Stihler electronic GMBH. Stuttgart, Germany)
and administering tempered fluids.Animals were premedicated with IM diazepam (Valium, Roche Farma, Madrid, Spain) (0.1 mg/kg) and ketamine (Ketolar, Pfizer, Madrid, Spain) (10 mg/kg). Anesthesia was induced with propofol (4 mg/kg), which was administered
after oxygenation by facial mask with 100% oxygen for 3 minutes. When lack of
jaw tone, loss of swallowing, lack of head shaking, loss of palpebral and pain
reflexes, and ventromedial rotation of the eyes were all detected, endotracheal
intubation was performed with the tube connected to a semiclosed circular
anesthetic circuit attached to a ventilator (Ventilator 7800, Ohmeda, Madrid,
Spain). Sevoflurane administration started at 5%, which enabled us to rapidly
achieve 1.25 MAC (1MAC = 2.66%) [10] with an oxygen flow rate of 3 L/min. Once 1.25 MAC was
reached (3.3% Et sevoflurane), the vaporizer setting was adjusted as needed to
maintain this concentration. Muscle relaxation was obtained by injection of vecuronium (0.1 mg/kg) (Norcuron, Organon Española, Barcelona Spain)
every 30 minutes. A bolus (5 μg/kg)
of fentanyl (Fentanest, Roche, Madrid, Spain)
was administered every 30 minutes. Systemic heparinization (Heparina Rovi 5%,
laboratorios farmacéuticos Rovi SA, Madrid, Spain) was
administered (150 UI/kg) 5 minutes prior to aortic cross-clamping. Postoperative
analgesia was assured by administering 10 μg/Kg
of IM Buprenorphine (Buprex, Schering-Plough, Madrid, Spain)
every 8 hours.Intermittent positive pressure ventilation was used during the procedure to maintain
end-tidal CO2 concentration between 35 to 45 mmHg, with a tidal
volume of 10 mL/kg in the open surgery group and ranging between 13–15 mL/kg in the
laparoscopy groups.During surgery, continuous infusion of Ringer-lactate
solution (Ringer-lactato, Braun, Barcelona,
Spain) at a
rate of 10 mL/kg/h was administered. 500 mL of a colloid solution (hydroxyethyl
starch, Voluven 6%, Fresenius Kabi, Barcelona, Spain) was administered five minutes before declamping in every animal. At the end of the surgery, the vaporizer was switched off and fresh gas flow rate was increased to 10 L/min of 100% oxygen. Pigs were extubated when they regained swallowing
reflexes and considered recovered and fully conscious when the attending
anesthesiologists recorded their ability to stand and walk.


### 2.3. Surgical Procedures

For pigs undergoing laparotomy, a
standard ventral midline approach was used (Group I). For pigs undergoing
laparoscopy (Groups II and III), 3 10 mm laparoscopic ports were inserted. Pneumoperitoneum was created by insufflating CO2 into the abdominal
cavity; intra-abdominal pressure was maintained at 12 to 14 mm Hg in both groups (Groups II and III). In Group III, CO2 pneumoperitoneum was maintained for 120 minutes, which was considered the minimum time needed to complete the cross-clamping procedure performed in Group II.In animals belonging to Groups I and II, aortic dissection was performed from the origin of the renal arteries to the origin of the caudal mesenteric artery, and all
lumbar arteries in the target aortic segment were temporarily occluded. The
aorta was then cross-clamped immediately below the origin of the caudal renal
artery and immediately cranial to the inferior mesenteric artery. Aortic
occlusion was maintained for 60 minutes.These procedures were always performed by the same surgical team using the same technique in order to achieve reproducible stimulation.


### 2.4. Monitoring

BIS (A-1050TM, version 3.05.05, Aspect Medical Systems Inc, Natick, Mass, USA) was registered using a previously described electrodes montage [15]. Electrocardiography (Hewlett Packard model 86S,
Hewlett Packard, Geneva, Switzerland) (lead II) and pulse oximetry with a probe
(Clip Tip sensor, Oximeter Sensor, Datex-Ohmeda, Louisville, Colo, USA) placed
on the tongue were monitored. Other parameters registered were rectal
temperature, tidal volume, end-tidal concentration of sevoflurane, end-tidal CO2 concentration, and respiratory rate (Ohmeda RGM 5250, Ohmeda, Madrid, Spain). Muscle relaxation was observed and monitored by train-of-four (TOF) (TOF-Guard, Biometer International A/S, Odense, Denmark).Arterial blood pressure, central venous pressure and heart rate were also measured using a blood pressure module (Hewlett Packard Press M 1006B, Hewlett Packard, Geneva, Switzerland) connected to a system for monitoring hemodynamic variables.We measured hemodynamic variables in real time using the PulseCO continuous cardiac output monitoring system (LiDCO Ltd): cardiac
output (CO), stroke volume (SV) and systemic vascular resistance (SVR). The
system was calibrated using the lithium dilution technique [16] for cardiac
output measurement at a lithium dosage of 0.04 mL/kg.


### 2.5. Arterial Blood Gasometry Assays

Through the carotid artery, arterial blood was sampled at different times (see below). At each interval, 0.5 mL of blood were collected using a prefilled heparin syringe. pH, PaCO2,
PaO2 and bicarbonate (CO3H-) were measured using the arterial gas
analyzer (Radiometer Medical, model ABL77, Copenhagen, Denmark).


### 2.6. Renal Function Tests

Urine production was registered every 30 minutes,
along with seric urea and creatinine. The Pourcelot or renal resistive index
was also determined at these times (RI = peak systolic velocity− end diastolic velocity/peak systolic velocity) at the arcuate arteries of the corticomedullary
junction, using a Panther 2002 (B&K Medical, Herlev, Denmark) ultrasound
scanner with a conventional probe (5,5 MHz) for transcutaneous examination and
a 9.8 mm laparoscopic probe (6,5 MHz) for the laparoscopic approach.


### 2.7. Data Processing

All data were expressed as mean ± SD at the following times:T1
baseline (immediately after connecting the patient to the monitoring systems prior to surgery;T2
Groups I and
II, 5 minutes before cross-clamping. Group III pneumoperitoneum establishment;T3
Groups I and
II, 30 minutes after cross-clamping. Group III 60 minutes after
pneumoperitoneum creation;T4
Groups I and
II, 60 minutes after cross-clamping. Group III, 120 minutes after
pneumoperitoneum creation;T5
Groups I and
II, 5 minutes after declamping or 5 minutes after the end of pneumoperitoneum
in Group III;T6
Groups I and
II, 30 minutes after declamping or 30 minutes after the end of pneumoperitoneum
in Group III;T7
Groups I and
II, 60 minutes after declamping or 60 minutes after the end of pneumoperitoneum
in Group III.
A Kolmogorov Smirnov test [17] was used to determine that data were normally distributed. Changes in
ventilatory and hemodynamic variables at each time point were analyzed using
ANOVA for repeated measures followed by the Tukey test to examine intergroup
deviation from control values. Recovery times were analyzed by use of ANOVA, using
the group (laparotomy with cross-clamping, laparoscopy with cross-clamping, or
laparoscopy alone) as the independent variable. Values of P<.05
were considered significant (SPSS 14.0 statistical package for Windows, SPSS
Inc, Chicago, Ill, USA).


## 2.1. Animals

The experimental protocol was approved by the Institutional Ethical Committee for Animal Research. Eighteen healthy female large white pigs were used. Mean weight was30.8±2.0 kg.


## 2.2. Anesthesia

One day prior to the experimental anesthetic episode,
each pig was anesthetized with sevoflurane (Sevorane, Abbott Laboratories,
Madrid, Spain), and a 20-standard wire gauge catheter was placed in the carotid
artery and fixed to the skin. Similarly, on that same day a 4Fr. vascular
sheath was placed in the external jugular vein using the Seldinger technique.
Pigs were randomly assigned to 3 groups. Groups I(n=6) and II (n=6) underwent
aortic cross-clamping through either laparotomy in Group I or laparoscopy in
Group II. Animals belonging to Group III underwent a 120-minute long
laparoscopy in absence of aortic intervention (sham group). Food, but not water, was withheld for 8 hours
prior to surgery. Body temperature was maintained stable at 37-38ºC, using a
thermal blanket (Astopad system, Stihler electronic GMBH. Stuttgart, Germany)
and administering tempered fluids.Animals were premedicated with IM diazepam (Valium, Roche Farma, Madrid, Spain) (0.1 mg/kg) and ketamine (Ketolar, Pfizer, Madrid, Spain) (10 mg/kg). Anesthesia was induced with propofol (4 mg/kg), which was administered
after oxygenation by facial mask with 100% oxygen for 3 minutes. When lack of
jaw tone, loss of swallowing, lack of head shaking, loss of palpebral and pain
reflexes, and ventromedial rotation of the eyes were all detected, endotracheal
intubation was performed with the tube connected to a semiclosed circular
anesthetic circuit attached to a ventilator (Ventilator 7800, Ohmeda, Madrid,
Spain). Sevoflurane administration started at 5%, which enabled us to rapidly
achieve 1.25 MAC (1MAC = 2.66%) [10] with an oxygen flow rate of 3 L/min. Once 1.25 MAC was
reached (3.3% Et sevoflurane), the vaporizer setting was adjusted as needed to
maintain this concentration. Muscle relaxation was obtained by injection of vecuronium (0.1 mg/kg) (Norcuron, Organon Española, Barcelona Spain)
every 30 minutes. A bolus (5 μg/kg)
of fentanyl (Fentanest, Roche, Madrid, Spain)
was administered every 30 minutes. Systemic heparinization (Heparina Rovi 5%,
laboratorios farmacéuticos Rovi SA, Madrid, Spain) was
administered (150 UI/kg) 5 minutes prior to aortic cross-clamping. Postoperative
analgesia was assured by administering 10 μg/Kg
of IM Buprenorphine (Buprex, Schering-Plough, Madrid, Spain)
every 8 hours.Intermittent positive pressure ventilation was used during the procedure to maintain
end-tidal CO2 concentration between 35 to 45 mmHg, with a tidal
volume of 10 mL/kg in the open surgery group and ranging between 13–15 mL/kg in the
laparoscopy groups.During surgery, continuous infusion of Ringer-lactate
solution (Ringer-lactato, Braun, Barcelona,
Spain) at a
rate of 10 mL/kg/h was administered. 500 mL of a colloid solution (hydroxyethyl
starch, Voluven 6%, Fresenius Kabi, Barcelona, Spain) was administered five minutes before declamping in every animal. At the end of the surgery, the vaporizer was switched off and fresh gas flow rate was increased to 10 L/min of 100% oxygen. Pigs were extubated when they regained swallowing
reflexes and considered recovered and fully conscious when the attending
anesthesiologists recorded their ability to stand and walk.


## 2.3. Surgical Procedures

For pigs undergoing laparotomy, a
standard ventral midline approach was used (Group I). For pigs undergoing
laparoscopy (Groups II and III), 3 10 mm laparoscopic ports were inserted. Pneumoperitoneum was created by insufflating CO2 into the abdominal
cavity; intra-abdominal pressure was maintained at 12 to 14 mm Hg in both groups (Groups II and III). In Group III, CO2 pneumoperitoneum was maintained for 120 minutes, which was considered the minimum time needed to complete the cross-clamping procedure performed in Group II.In animals belonging to Groups I and II, aortic dissection was performed from the origin of the renal arteries to the origin of the caudal mesenteric artery, and all
lumbar arteries in the target aortic segment were temporarily occluded. The
aorta was then cross-clamped immediately below the origin of the caudal renal
artery and immediately cranial to the inferior mesenteric artery. Aortic
occlusion was maintained for 60 minutes.These procedures were always performed by the same surgical team using the same technique in order to achieve reproducible stimulation.


## 2.4. Monitoring

BIS (A-1050TM, version 3.05.05, Aspect Medical Systems Inc, Natick, Mass, USA) was registered using a previously described electrodes montage [15]. Electrocardiography (Hewlett Packard model 86S,
Hewlett Packard, Geneva, Switzerland) (lead II) and pulse oximetry with a probe
(Clip Tip sensor, Oximeter Sensor, Datex-Ohmeda, Louisville, Colo, USA) placed
on the tongue were monitored. Other parameters registered were rectal
temperature, tidal volume, end-tidal concentration of sevoflurane, end-tidal CO2 concentration, and respiratory rate (Ohmeda RGM 5250, Ohmeda, Madrid, Spain). Muscle relaxation was observed and monitored by train-of-four (TOF) (TOF-Guard, Biometer International A/S, Odense, Denmark).Arterial blood pressure, central venous pressure and heart rate were also measured using a blood pressure module (Hewlett Packard Press M 1006B, Hewlett Packard, Geneva, Switzerland) connected to a system for monitoring hemodynamic variables.We measured hemodynamic variables in real time using the PulseCO continuous cardiac output monitoring system (LiDCO Ltd): cardiac
output (CO), stroke volume (SV) and systemic vascular resistance (SVR). The
system was calibrated using the lithium dilution technique [16] for cardiac
output measurement at a lithium dosage of 0.04 mL/kg.


## 2.5. Arterial Blood Gasometry Assays

Through the carotid artery, arterial blood was sampled at different times (see below). At each interval, 0.5 mL of blood were collected using a prefilled heparin syringe. pH, PaCO2,
PaO2 and bicarbonate (CO3H-) were measured using the arterial gas
analyzer (Radiometer Medical, model ABL77, Copenhagen, Denmark).


## 2.6. Renal Function Tests

Urine production was registered every 30 minutes,
along with seric urea and creatinine. The Pourcelot or renal resistive index
was also determined at these times (RI = peak systolic velocity− end diastolic velocity/peak systolic velocity) at the arcuate arteries of the corticomedullary
junction, using a Panther 2002 (B&K Medical, Herlev, Denmark) ultrasound
scanner with a conventional probe (5,5 MHz) for transcutaneous examination and
a 9.8 mm laparoscopic probe (6,5 MHz) for the laparoscopic approach.


## 2.7. Data Processing

All data were expressed as mean ± SD at the following times:T1
baseline (immediately after connecting the patient to the monitoring systems prior to surgery;T2
Groups I and
II, 5 minutes before cross-clamping. Group III pneumoperitoneum establishment;T3
Groups I and
II, 30 minutes after cross-clamping. Group III 60 minutes after
pneumoperitoneum creation;T4
Groups I and
II, 60 minutes after cross-clamping. Group III, 120 minutes after
pneumoperitoneum creation;T5
Groups I and
II, 5 minutes after declamping or 5 minutes after the end of pneumoperitoneum
in Group III;T6
Groups I and
II, 30 minutes after declamping or 30 minutes after the end of pneumoperitoneum
in Group III;T7
Groups I and
II, 60 minutes after declamping or 60 minutes after the end of pneumoperitoneum
in Group III.
A Kolmogorov Smirnov test [17] was used to determine that data were normally distributed. Changes in
ventilatory and hemodynamic variables at each time point were analyzed using
ANOVA for repeated measures followed by the Tukey test to examine intergroup
deviation from control values. Recovery times were analyzed by use of ANOVA, using
the group (laparotomy with cross-clamping, laparoscopy with cross-clamping, or
laparoscopy alone) as the independent variable. Values of P<.05
were considered significant (SPSS 14.0 statistical package for Windows, SPSS
Inc, Chicago, Ill, USA).


## 3. Results

Mean± SD duration of anesthesia was 216 ± 15 minutes in the animals that underwent laparotomy,
367 ±
24 minutes in the laparoscopic cross-clamping group and 195 ± 26
minutes in Group III. The difference between Groups I and II was mainly
attributable to the different time needed to complete aortic dissection (12 ± 4
minutes for pigs undergoing laparotomy versus 39 ± 4 minutes for pigs undergoing laparoscopy) plus the time needed for placing the lumbar clips and the aortic clamps.SpO2 was >97% and EtCO2 was maintained between 35 to 40 mmHg in all
pigs. Blood loss was minimal for all procedures.Anesthetic
depth, as determined by BIS [18] and clinical observation was consistent with a
surgical plane of anesthesia.The changes observed in all the measured variables are reflected in Tables1, 2, 3, 4, 5, and 6. In brief, these changes are summarized below.Table 1
Heart rate and
mean arterial blood pressure in pigs anesthetized with sevoflurane, fentanyl,
and vecuronium and undergoing aortic cross-clamping through laparotomy (Group
I) or laparoscopy with (Group II) or without aortic cross-clamping (Group III).
Heart rate (beats/min)Mean arterial blood pressure (mmHg)TimesGroup IGroup IIGroup IIIGroup IGroup IIGroup IIIT179.6±11.781.6±11.076.5±3.168.2±7.357.6±1.865.7±10.6T278.8±14.485.8±12.378.5±4.265.0±7.473.0±6.4*81.7±10.1*T378.7±14.486.8±14.878.7±4.178.8±13.8*77.0±9.1*84.3±8.5*T482.8±18.788.0±18.078.0±6.283.2±15.8*78.8±8.2*85.2±7.5*T589.8±21.2100.0±22.778.5±7.052.6±12.0*61.8±9.376.0±15.7T690.7±15.394.0±16.280.2±8.364.7±7.752.6±4.968.8±18.1T793.0±15.391.4±11.978.3±7.464.8±8.053.6±5.468.7±16.2Data are expressed as mean± SD.*Significant
changes from baseline (P<.05).Table 2
Central venous pressure (CVP), cardiac
output (CO) in pigs anesthetized with sevoflurane, fentanyl, and vecuronium and
undergoing aortic cross-clamping through laparotomy (Group I) or laparoscopy
with (Group II) or without aortic cross-clamping (Group III).
CVP (cm H2O)CO (L/min)TimesGroup IGroup IIGroup IIIGroup IGroup IIGroup IIIT15.3±1.43.6±0.54.0±0.54.16±0.614.06±0.623.57±0.48T25.0±1.86.4±3.2*7.3±1.2*4.13±0.523.49±0.733.08±0.36T34.2±2.16.2±3.4*6.6±0.4*4.12±1.042.80±1.21*2.67±0.15*T45.8±2.74.8±2.55.5±0.63.40±1.213.12±1.42*2.88±0.26T54.8±3.24.8±3.53.4±1.66.50±2.12*5.50±1.88*3.18±0.40†T65.5±3.01.6±0.52.7±0.95.28±1.674.88±1.863.40±0.67†T75.8±2.62.6±1.52.6±1.54.90±1.114.54±1.013.45±0.60†Data are expressed as mean± SD.*Significant
changes from baseline (P<.05).Table 3
Systolic volume (SV) and
and systemic vascular resistance (SVR) in pigs
anesthetized with sevoflurane, fentanyl, and vecuronium and undergoing aortic
cross-clamping through laparotomy (Group I) or laparoscopy with (Group II) or
without aortic cross-clamping (Group III).
SV (mL)SVR (Dyn s/cm5)TimesGroup IGroup IIGroup IIIGroup IGroup IIGroup IIIT149.0±10.542.2±20.042.5±0.51556± 3701460± 3591735± 202T245.8±9.735.2±10.341.5±3.51509± 3941940± 529*2098± 133*T338.0±11.137.2±13.636.8±2.62083± 456*2080± 957*2455± 397*T439.5±15.438.0±12.636.0±2.42100± 610*2010± 1016*2508± 469*T562.2±25.4*62.0±33.3*44.0±5.5933± 513*1160± 2901926± 410T651.5±17.743.0±33.941.0±1.51208± 4831230± 2562032± 482T752.3±14.545.6±15.942.7±1.91361± 6361320± 971880± 337*Significant changes from baseline (P<.05).Table 4
Acid-base balance in pigs
anesthetized with sevoflurane, fentanyl, and vecuronium and undergoing aortic
cross-clamping through laparotomy (Group I) or laparoscopy with (Group II) or
without aortic cross-clamping (Group III).
pHCO3H- (mmol/L)TimesGroup IGroup IIGroup IIIGroup IGroup IIGroup IIIT17.48±0.017.47±0.017.40±0.7326.7±3.331.2±1.130.1±0.9T27.43±0.027.32±0.077.40±0.0423.1±7.327.4±5.7×30.0±1.4×T37.46±0.047.27±0.16*†7.40±0.520.6±4.331.2±3.5×31.0±1.5×T47.46±0.057.28±0.17*†7.40±0.126.6±2.333.8±2.3×30.8±1.3×T57.40±0.067.22±0.18*†7.43±0.124.1±3.429.1±7.1×30.3±1.7×T67.41±0.067.34±0.077.38±0.624.7±3.232.8±3.6×30.0±1.6×T77.38±0.017.32±0.077.34±0.121.5±7.632.5±4.0×30.3±1.6×*Significant changes from baseline (P<.05).†Significantly (P<.05)
different from values for pigs undergoing laparoscopy and cross-clamping.×Significantly (P<.05)
different from values for pigs undergoing laparoscopy.Table 5
Acid-base balance in pigs
anesthetized with sevoflurane, fentanyl, and vecuronium and undergoing aortic
cross-clamping through laparotomy (Group I) or laparoscopy with (Group II) or
without aortic cross-clamping (Group III).
PaCO2 (mmHg)PaO2 (mmHg)TimesGroup IGroup II†Group IIIGroup IGroup IIGroup IIIT136.0±5.041.1±3.738.0±2.4487.8±99.3574.2±81.1501.2±41.7T233.0±9.245.6±6.443.0±6.5447.3±111.7370.6±88.2*495.7±37.3T330.7±6.148.1±3.8*43.0±3.9443.7±34.8399.8±96.3*479.0±33.2T437.5±6.951.6±2.3*43.7±3.0501.7±64.9392.6±110.5*456.7±48.6T539.5±7.249.0±4.4*42.2±2.2497.0±58.2458.2±106.2445.0±47.6T637.8±7.048.6±4.0*39.2±2.2481.0±72.7440.0±105.4448.7±26.6T738.5±8.546.0±2.238.0±2.3434.3±76.9452.0±106.9462.0±16.9Data are expressed as mean± SD.†Significantly (P<.05)
different from values obtained for pigs undergoing laparoscopy and cross-clamping.*Significant changes from baseline within each group (P<.05).Table 6
Renal resistive index values
obtained thorough the study.
T1T2T3T4T5T7Group I0.48± 0.03—0.58± 0.110.63± 0.070.56± 0.100.53±0.10Group II0.53± 0.100.69±0.05*†0.69± 0.06*†0.68± 0.08*†0.68± 0.02*†0.56±0.02Group III0.49± 0.030.58±0.03*0.58± 0.11*0.64± 0.03*0.60± 0.10*0.49±0.02†Significantly (P<.05)
different from values obtained for pigs undergoing laparoscopy and cross-clamping.*Significant changes from baseline within each group (P<.05).Immediate and significant increases in ABP and SRV
and decreases in CO and SV following aortic cross-clamping, without any
concurrent significant changes to CVP or heart rate, were seen in Groups I and
II (Tables1, 2, and 3). After declamping
(T5), a significant increase in CO and SV and a significant decrease in ABP and
SVR were also observed.In Groups II and III, pneumoperitoneum caused a significant increase in CVP, ABP, and SVR along
with decreased CO (Tables1, 2, and 3). In Group II a significant increase in
PaCO2 and a significant decrease in pH (Table 4) were seen.No significant changes in pH or arterial gasometry were caused by clamping or declamping in
Group I, whereas in Group II a further significant decrease in pH values was
seen during cross-clamping, whilst HCO3 was kept over 26 mmol/l during cross-clamping
and declamping in order to compensate for the acidosis (Tables4 and 5).No significant changes in urea or
creatinine were evidenced between groups. However, significant(P<.05)
increases in the RI were seen during infrarenal aortic cross-clamping in Group
II (laparoscopy) (Table 6) and during pneumoperitoneum creation in Group III,
with the increase being significantly greater in Group II than in Group III.
Similarly, urine production was decreased by 35% during laparoscopic clamping
when compared to cross-clamping by open surgery, and by 30% during
laparoscopic cross-clamping when compared to laparoscopy in absence of aortic
cross-clamping.60 minutes after declamping, all the studied variables
had returned to baseline values in all groups. No significant differences were
observed between groups in regard to recovery times except for the time to
standing which was significantly lower in Groups II and III (pigs that had
undergone laparoscopy) (Table7).Table 7
Recovery times
in pigs anesthetized with sevoflurane, fentanyl, and vecuronium and undergoing
aortic cross-clamping through laparotomy (Group I) or laparoscopy with (Group
II) or without aortic cross-clamping (Group III).
Recovery time (min)Recovery
indicatorGroup IGroup IIGroup IIIFirst
movement12.5±8.212.6±10.510.5±3.5*Extubation11.6±5.811.2±4.17.5±1.0Sternal
recumbency34.7±23.837.4±14.127.2±2.3Standing292.2±14.771.6±20.1*79.3±15.9**Significantly (P<.05)
different from values obtained for pigs undergoing laparoscopy.


## 4. Discussion

While the systemic cardiovascular consequences of infrarenal aortic cross-clamping during
aortic abdominal surgery are well documented in both humans [9] and pig [19], and have been
reported to be very similar (this
animal model reproduces the changes observed in humans), its
repercussions during laparoscopic surgery have not been reported.In the present study, pneumoperitoneum caused a significant increase in arterial blood pressure and systemic vascular resistance. Generally speaking, the higher
arterial blood pressure observed may be attributed to the increase in
intra-abdominal pressure caused by pneumoperitoneum, which gives rise to
increased systemic vascular resistance and arterial blood pressure to
compensate for the decrease in cardiac output secondary to the decreased venous
return [2].
However other authors have reported that neither increased intra-abdominal pressure
nor plasma accumulation of carbon dioxide influences cardiac output [20, 21]. In this study, a decrease in cardiac output was evidenced immediately after
pneumoperitoneum creation. In our opinion, hypertension may also be caused by
any of three factors: mechanical compression of the splanchnic vascular bed; a
sympathetic reflex from the splanchnic regions; and the release of humoral
vasoconstriction mediators, such as renin or vasopressin [21–23]. Systemic arterial hypertension has consistently been found during inflation of the peritoneum with CO2, but Huang et al. [24] reported that hypercarbia might not be the major determinant factor of it.Cross-clamping of the aorta also caused a marked increase in arterial blood pressure, most likely due to the sudden increase in impedance to aortic blood flow and the resultant increase in systolic   ventricular wall tension or afterload. However, factors such as myocardial contractility, preload, blood volume, and sympathetic nervous system activation may also be important [25].Although several clinical reports have noted no significant hemodynamic response to infrarenal cross-clamping [26, 27], the hemodynamic response generally consists of increases in arterial pressure (7 to 10%) and systemic vascular resistance (20 to 32%) with no significant change in heart rate [9–11, 28]. Cardiac output is generally decreased by 9% to 33% [27]. Reported changes in ventricular filling
pressures have been inconsistent [12, 27, 29]. Changes in these parameters seen in both groups, in the present study, followed a similar pattern.Despite the increase in ABP and SVR and the decrease in CO brought over by pneumoperitoneum creation, these variables’ values were similar in Groups I and II during aortic cross-clamping. In our opinion, aortic cross-clamping did not greatly affect hemodynamic changes secondary to pneumoperitoneum, as shown by the fact that
these variables changed in absence of cross-clamping in Group III.Regarding ventilatory changes, it is known that if correct ventilatory support is
provided, SpO2 can easily be maintained >90% during laparoscopy. Carbon dioxide
pneumoperitoneum causes absorption of this gas, and if lung ventilation is
insufficient to eliminate the absorbed carbon dioxide, hypercapnia will develop,
which may cause acidosis, depress myocardial function, and induce arrhythmias
and cardiovascular collapse [2]. In view of this possibility, controlled ventilation
was used in the present study to prevent hypercapnia, and minute ventilation
was adjusted to maintain EtCO2 at 35–40 mmHg
throughout the entire procedure, increasing by approximately 30% (minute
ventilation before laparoscopy was 3.6±0.2 L/min, and it reached 4.9 ±
0,5 L/min during laparoscopy) and maintaining a ventilatory rate of 10–12 breaths/min,
as has been previously reported [30, 31]. Prior studies [20] reported that insufflation of the
peritoneal cavity with CO2 to an intra-abdominal pressure <15
mmHg does not interfere significantly with pulmonary gas exchange in patients
without preexisting cardiopulmonary diseases. Other authors reported a
statistically significant correlation between PaCO2 and EtCO2 during 60 minutes of CO2 insufflation [32]. A significant decrease
in pH and concomitant increase in PaCO2 were seen in Group II after clamping, whereas they remained stable in the other
two groups at the same time points. These parameters remained changed in this
group whilst the aorta was clamped, and they did not regain baseline values
until 30 minutes (pH) or 60 minutes (PaCO2)
after declamping. This could be attributed to the combined effect of aortic
clamping and pneumoperitoneum, which could lead to the development of an
acidosis of mixed metabolic and respiratory origin. The acidosis seen in Group
II was not compensated by the
above described ventilatory changes, therefore causing increased bicarbonate
values and leading us to consider this mixed metabolic and hypercarbic origin
for the acidosis, supporting the prior studies of Tobias et al. [33].An increase in
the partial pressure of arterial carbon dioxide was evidenced in this study. In
our opinion, it can be due to CO2 absorption, rather than to the
mechanical ventilatory repercussions of increased intra-abdominal pressure [34–36]. It has been previously
described that, in healthy patients, absorption of CO2 from the
abdominal cavity represents the main (or the only) mechanism responsible for
increased PaCO2
[37].
However, in cases of cardiorespiratory compromise, ventilatory changes also
contribute significantly to increasing PaCO2
[38]. Therefore, although
increased PaCO2 may be well tolerated by young and healthy patients,
the extent to which hypercapnia is acceptable has not been determined and
probably varies according to the patient’s physical status. It is thus wise to
maintain PaCO2 within physiologic ranges by adjusting controlled
mechanical ventilation [39].Acute renal failure
requiring dialysis is a severe complication in up to 5% of open aortic
surgeries, and it causes high mortality rate [40]. No data
about renal failure during laparoscopic aortic surgery could be found in the
literature. However, the increased RI evidenced during
laparoscopy in this study, both with and without aortic clamping, suggests that
its incidence may be higher in this approach than in conventional aortic
surgery. There are multiple factors involved in renal failure. On the one hand,
aortic cross-clamping elicits marked hemodynamic changes that impact kidney
function, increasing renal vascular resistance and markedly decreasing blood
flow to the renal cortex [37]. On the other hand, the increased intra-abdominal pressure
secondary to CO2 insufflation markedly contributes to the significant decrease
in renal flow [41], due to vascular
compression at the renal parenchyma and the decreased cardiac output seen in
the groups undergoing laparoscopy. Despite the absence of permanent renal
injury after aortic cross-clamping in either group, careful patient selection
for procedures involving laparoscopic aortic cross-clamping is warranted,
specially in patients presenting with preexisting nephropathies to avoid
further deterioration of their condition.Recovery was
swift in the present study. Mean time to standing was significantly lower in
Groups II and III (laparoscopy). This is probably attributable to a lesser
degree of postoperative pain in animals subjected to laparoscopic surgery, as
suggested by the fact that patients subjected to a laparotomy generally
complain more of parietal pain (abdominal wall) whereas after laparoscopy,
visceral pain is normally present [42].To our knowledge, we report the first study
concerning the physiologic changes occurring during infrarenal aortic surgery
using laparoscopic technique. Hemodynamic management of aortic cross-clamping
was similar for both surgical approaches in pig [43], however, aortic cross-clamping during laparoscopy causes mixed respiratory and metabolic acidosis that needs to be monitored by arterial gas analysis, even in the
absence of abnormal EtCO2 levels, along with an increasing renal vascular
resistance and markedly decreasing blood flow to the renal cortex.
Despite being compensated and well tolerated in healthy pigs, this acidosis
must be corrected by adjusting controlled mechanical ventilation. Further studies in experimental
animal models [44] are required to determine the clinical implication of these findings and their
impact in the presence of cardiovascular comorbidity (aortic diseases, hypertension, coronary
artery disease, chronic obstructive pulmonary disease, etc.) during aortic
surgery.



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*Source: 581948-2008-03-27.xml*