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Revista Brasileira de Anestesiologia

Print version ISSN 0034-7094On-line version ISSN 1806-907X

Rev. Bras. Anestesiol. vol.55 no.6 Campinas Nov./Dec. 2005 



Hemodynamic and ventilatory effects of volume or pressure controlled ventilation in dogs submitted to pneumoperitoneum. Comparative study*


Estudio comparativo de los efectos hemodinámicos y ventilatorios de la ventilación controlada a volumen o a presión, en perros sometidos a pneumoperitoneo



Antonio Roberto Carraretto, TSA, M.D.I; Pedro Thadeu Galvão Vianna, TSA, M.D.II; Armando Vieira de Almeida, TSA, M.D.I; Eliana Marisa Ganem, TSA, M.D.III

IPós-Graduando (Mestrado) do Programa de Pós-Graduação em Anestesiologia da FMB UNESP
IIProfessor Titular do CET/SBA do Departamento de Anestesiologia da FMB UNESP
IIIProfessora Adjunta Livre-Docente do CET/SBA do Departamento de Anestesiologia da FMB UNESP

Correspondence to




BACKGROUND AND OBJECTIVES: Pressure controlled ventilation (PCV) is available in anesthesia machines, but there are no studies on its use during CO2 pneumoperitoneum (CPP). This study aimed at evaluating pressure-controlled ventilation and hemodynamic and ventilatory changes during CPP, as compared to conventional volume controlled ventilation (VCV).
METHODS: This study involved 16 dogs anesthetized with thiopental, fentanyl and pancuronium, which were randomly assigned to two groups: VC - volume controlled ventilation (n=8) and PC - pressure controlled ventilation (n=8). Hemodynamic and ventilatory parameters were monitored and recorded in 4 moments: M1 (before CPP), M2 (30 minutes after CPP = 10 mmHg), M3 (30 minutes after CPP=15 mmHg) and M4 (30 minutes after deflation).
RESULTS: With CPP, there has been significant increase in tidal volume in PC group; there has been increase in airway pressures (peak and plateau), decrease in compliance with increase in CPP pressure, increase in heart rate, maintenance of mean blood pressure with higher values in the VC group in all stages; there was also increase in right atrium pressure with significant decrease after deflation, decrease in arterial pH with minor variations in PC group, greater arterial pCO2 stability in PC group, and no significant changes in arterial pO2.
CONCLUSIONS: There were some differences in hemodynamic and ventilatory data between both ventilation control modes (VC and PC). It is possible to use pressure controlled ventilation during CPP, but the anesthesiologist must monitor and take a close look at alveolar ventilation, adjusting inspiratory pressure to ensure proper CO2 elimination and oxygenation.

Key words: ANIMAL, Dog; SURGERY, Abdominal: videolaparoscopic; VENTILATION: mechanically controlled


JUSTIFICATIVA Y OBJETIVOS: La ventilación con presión controlada (PCV) está disponible en aparatos de anestesia, pero no existen estudios sobre su uso, durante el pneumoperitoneo con el CO2 (PPC). La finalidad de este estudio ha sido evaluar la ventilación controlada a presión, también como las alteraciones hemodinámicas y ventilatorias durante el PPC, comparándola con la ventilación controlada a volumen (VCV) convencionalmente utilizada.
MÉTODO: Dieciséis perros anestesiados con tiopental sódico, citrato de fentanil y bromuro de pancuronio, fueron divididos eventualmente en dos grupos: VC - ventilación controlada a volumen (n = 8) y PC - ventilación controlada a presión (n = 8) Los parámetros hemodinámicos y ventilatorios fueron monitorizados y registrados en 4 momentos: M1 (antes del PPC), M2 (30 minutos después del PPC = 10 mmHg), M3 (30 minutos después del PPC = 15 mmHg) y M4 (30 minutos después de la deflación del PPC).
RESULTADOS: Con la aplicación del PPC ocurrió un aumento del volumen corriente en el grupo PC, aumento de las presiones inspiratorias (máxima y de plato), disminución de la complacencia proporcional al aumento del PPC, aumento de la frecuencia cardiaca, mantenimiento de la presión arterial media con valores mayores en el grupo VC en todos los momentos, aumento de la presión del atrio derecho con disminución significativa después de la deflación, disminución del pH sanguíneo durante el PPC con menor variación en el grupo PC, mayor estabilidad de la presión parcial del CO2 en la sangre arterial en el grupo PC, sin alteraciones de la presión parcial de la O2 en la sangre arterial.
CONCLUSIONES: A pesar de las diferencias de algunos parámetros hemodinámicos y ventilatorios, entre los dos modos de control de la ventilación, en las condiciones estudiadas fue posible la utilización de la ventilación controlada a presión para procedimientos con la aplicación del PPC. Es fundamental observar el control riguroso de la ventilación alveolar, ajustando la presión inspiratoria para mantener una eliminación adecuada del CO2 y garantizar oxigenación.




Videolaparoscopy is beneficial for patients and health systems and its use is increasing in number and complexity. It is necessary to expand the abdominal cavity in order to visualize the content and operate the instruments. Most common technique is carbon dioxide (CO2) inflation to create pneumoperitoneum. Although the presence of CO2 in the metabolic system, absorption and increased blood concentration above certain values promotes cardiovascular effects such as increased cardiac output 1,2, increased mean blood pressure, and increased plasma epinephrine and norepinephrine concentrations1. Its vasodilating effect may lead to systemic vascular resistance (SVR) decrease when not compensated by venous capacitance system through the sympathetic nervous system 1,2. Reports on CO2 inhalation effects on the ventilatory mechanics of non-anesthetized individuals spontaneously breathing are controversial. Airways resistance may be increased 3, decreased 4 or unchanged 5.

Increased intra-abdominal pressure has mechanical effects on abdomen and chest with cardiovascular and ventilatory changes, shifts the diaphragm in the cephalad direction, increases intra-thoracic pressure, lungs expansion is restricted by the shift of the abdominal part of the chest wall, dynamic pulmonary compliance decreases approximately 50%, and Paw peak and Paw plat are increased6-8.

General anesthesia induces ventilatory changes, which need controlled ventilation. Most ventilators installed in anesthesia machines have volume-controlled ventilation (VC) and pressure limited ventilation (PLV). New imported and some domestic equipment are starting to incorporate pressure-controlled ventilation (PC) already present and common in Intensive Care Units (ICU). Adjusted parameters in VC are inspiratory volume and flow, both flow peak and shape. Ventilatory rate and the ratio between inspiratory and expiratory times (I:E ratio) are dependent on these adjustments.

Airways pressure is dependent on system's resistance and compliance. In LVP, adjusted parameters are limit pressure and inspiratory flow. Volume is dependent on resistance and compliance. Depending on the cycling mechanism, I:E ratio and respiratory rate may change. In PC, adjusted parameters are: airways pressure, inspiratory time or I:E ratio and ventilatory rate. These parameters affect inspiratory flow and tidal volume profiles, which should be monitored for adequate ventilation. Modern ICU ventilators have the PC modality and have been studied in acute respiratory distress syndrome (ARDS) patients.

Sometimes these patients are transferred from the ICU to the Operating Theater and there is a request to continue with the same ventilation modality. The described ventilation modalities allow the addition of positive end expiratory pressure (PEEP), to prevent or decrease collapse and improve alveolar recruitment. Hemodynamic 9,10 and renal changes were evaluated by other studies with similar methods. This study aimed at evaluating the applicability of pressure-controlled ventilation (PC) in anesthesia in the presence of CO2 pneumoperitoneum, by measuring hemodynamic and ventilatory parameters and comparing them to conventional volume controlled ventilation (VC).



After the Animal Research Ethics Committee, Faculdade de Medicina, Botucatu - UNESP approval, 16 adult mixed breed dogs of both genders, weighing 15 to 23 kg, supplied by the Lab Animals Facility of the Botucatu Campus, UNESP were involved in this study. Animals were in fast for 12 hours with free access to water. Animals were randomly distributed in two groups of 8: VC group - volume controlled ventilation; and PC group - Pressure controlled ventilation (PC).

Experimental sequence: 1) Equipment check, test and adjustment (anesthesia machine, monitoring, infusion pumps, solutions heater, animal heater, gas inflator; 2) Recording of animals' weight, length and gender; 3) Anesthetic induction with intravenous sodium thiopental (15, fentanyl (0.015 and pancuronium (0.07; 4) Tracheal intubation (TI) with cuffed endotracheal tube (8.5 mm ID) and checking; 5) Connection of Biomonitor Datex AS3® adapter to the Y connector of the CO2 absorber filter of the anesthesia machine Ohmeda Excel 210 SE®, with fresh gases flow (FGF) = 0.5 L.min-1 of 100% oxygen (FIO2 = 1.0), to measure ventilation and analyze inspired and expired gases; 6) Beginning of mechanically controlled ventilation with Ohmeda 7900 ventilator coupled to the anesthesia machine in the selected modality, VC or PC, determined by the group, and adjustment of parameters to maintain desired ventilatory stability; 7) Installation of noninvasive monitoring: continuous ECG at DII lead, pulse oximeter and esophageal thermometer probe; 8) Right femoral vein dissection and catheterization for fluid and drug infusion and beginning of intravenous hydration with 6 Ringer's solution, through infusion pump and heater with temperature control at 36.5 ºC; 9) left femoral vein dissection and catheterization to monitor mean blood pressure (MBP) and blood collection for blood gases analysis, connected to the measurement transducer of previously gauged Datex AS3® monitor; 10) Right jugular vein dissection to introduce 7F Swan-Ganz catheter until the pulmonary artery for hemodynamic measures; 11) Median minilaparotomy to introduce 14F polyethylene catheter for gas inflation and IAP control, with Olympus Surgical Inflator 15-L® and gas removal at moment M3; 12) Animal covering with warming blanket by warm air inflation (42 - 46 ºC) using WarmTouch® equipment.

Anesthesia was maintained with thiopental (6 and fentanyl (0.006 in continuous infusion with ANNE® infusion pump. Additional pancuronium (0.02 and fentanyl (0.005 doses were administered when needed.

CO2 inflation in the abdominal cavity, to reach 10 mmHg IAP (after M1) and 15 mmHg (after M2) and gas removal for 0 mmHg IAP (after M3).

Animals were sacrificed at the end of experiment with 10 mL of intravenous 19.1% potassium chloride.

The following attributes were evaluated: weight (kg), length (cm) body surface (calculated - m2), gender (M/F), respiratory rate (r - mov.min-1 tidal volume (VT - mL), peak inspiratory pressure (Paw peek - cmH2O), plateau inspiratory pressure (Paw plat - cmH2O), chest compliance (CT - H2O), end tidal CO2 (PETCO2 - mmHg), heart rate (HR - beat.min-1), mean blood pressure (MBP - mmHg), mean right atrium pressure (RAP - mmHg), arterial pCO2 (PaCO2 - mmHg), and arterial pO2 (PaO2 - mmHg).

After catheter installation for CPP and monitoring, the 30-minute count was started looking for ventilatory stability by adjusting tidal volume (TV) or inspiratory pressure (PC) to maintain PETCO2 within desired limits (35 to 45 mmHg), with respiratory rate regulated to 10 ipm.min-1, I:E ratio = 1:2 and PEEP of 3 cmH2O. Ventilatory measures were obtained with Datex AS3® monitor with the probe close to the tracheal tube connector. This procedure has been previously validated 11.

Ventilatory, hemodynamic, blood and temperature measures were collected in moments M1, M2, M3 and M4, being: M1 - immediately after the end of 30-minute stabilization period with IAP = 0 mmHg; M2 - 30 minutes after CPP with IAP = 10 mmHg; M3 - 30 minutes after CPP with IAP = 15 mmHg; M4 - 30 minutes after CPP with IAP = 0 mmHg.

Analysis of Variance was used for weight, length and body surface area to compare between groups.

Profile analysis was used for remaining variables evaluated in the four moments 13.



Weight, length and body surface area were not significantly different between groups and are shown in table I.

Tidal volumes, regulated to maintain PETCO2 between 35 and 45 mmHg were not significantly different between groups in each moment. Values were constant for the VC group and increased for PC group after pneumoperitoneum, not returning to baseline values (Figure 1).

Peak inspiratory pressure increased with IAP increase for both groups, with a trend to higher values for VC group in M1 and M4, and returning to baseline values after deflation (Figure 2).

Plateau inspiratory pressure has increased with IAP increase and has returned to baseline values after deflation, with similar behavior between groups (Figure 3).

Compliance values have decreased with increased IAP in both groups. After deflation, VC group has returned to baseline values and PC group has remained with higher values (Figure 4).

End tidal CO2 was higher for VC group as compared to PC group during pneumoperitoneum, returning to baseline values after deflation. PC group presented greater uniformity of values (Figure 5).

Heart rate had the same behavior for both groups, with higher values in M2 and M3 (Figure 6).

Mean blood pressure was higher for VC group as compared to PC group. There were no differences among moments for both groups (Figure 7).

Right atrium pressure has increased during pneumoperitoneum and has decreased after deflation, with significant decrease in PC group (Figure 8).

Blood pH was different among moments. In VC group it decreased during pneumoperitoneum. In PC group it had less variation (Figure 9).

Arterial pCO2 was different between groups with increase (M2) and trend to increase (M3) in VC group during pneumoperitoneum, and stability in PC group (Figure 10).

Arterial pO2 had the same behavior, without differences between groups and moments (Figure 11).



Among major available controls during mechanically controlled ventilation there are volume and pressure, object of our study. These may be individually or jointly preset, generating volume controlled ventilation (VCV) or pressure controlled ventilation (PCV). Control combinations, such as target volume, pressure controlled and time cycling are among new available modalities called double control modes.

In our study, to better control different evaluated parameters, respiratory rate was established in 10 mov.min-1, similar to other studies 7,14, and I:E ratio in 1:2. These values allowed adequate animals ventilation, confirmed by values obtained from PETCO2, PaCO2 and PaO2 analyses.

Tidal volume had to be increased by adjusting volume control in VC group or pressure control in PC group, to maintain PETCO2 within desired values. A different study has shown the need to increase respiratory minute volume, from 20% to 30%, to eliminate absorbed CO2 by CPP 15.

In VCV, the volume to be administered is a fixed parameter (predetermined) together with ventilatory rate and I:E ratio. The ventilator generates a controlled flow, which is interrupted at the end of inspiration. After it, there may be an inspiratory pause (with maintenance of plateau pressure) or the cycling to the expiratory phase. Pressure will be the result of ventilatory mechanics, such as changes on resistance and compliance. With increased IAP, increased intra-thoracic pressure increases airways pressure. Minute volume suffers minor or no change and alveolar ventilation, responsible for alveolar CO2 removal, is maintained.

In PCV, the ventilator starts the cycle with a demand flow needed to maintain a predetermined pressure (fixed parameter). When this pressure is reached, the flow is gradually decreased (slow down flow) to maintain the pressure. Tidal volume depends on regulated pressure, inspiratory time and, as in any pressure mode, will be influenced by ventilatory mechanics changes (compliance and resistance) 16.

During PCV, at inspiratory valve opening, gas flow is high and most volume is distributed in the beginning of the inspiratory phase. Pressure control valve regulates the inspiratory flow maintaining the pressure constant e allowing a better gas distribution to alveoli with higher time constant without promoting hyperdistension - by controlling alveolar pressure. Increased ventilatory rate or inspiratory pressure are needed to improve alveolar ventilation

Increased airways resistance or decreased pulmonary compliance decrease tidal volume and, as a consequence, alveolar ventilation. Due to IAP effects on intra-thoracic pressure, each IAP variation may need correction of ventilatory parameters, in general a new pressure, to compensate the effect of tidal volume loss or gain.

In a comparative study between PCV and VCV, in patients with severe acute respiratory distress syndrome (ARDS), it has been observed less cardiac output decrease in the PCV group, reported as the result of right ventricle overload improvement due to better alveolar recruitment, decreased pulmonary vascular resistance and decreased intra-thoracic pressure, which has helped a better preload of both ventricles 17.

A different comparative study with patients submitted to single-lung ventilation has observed significantly higher Paw peak, Paw plat and pulmonary shunt during VCV, while PaCO2 was higher during PCV. The study has concluded that PCV is an alternative to VCV in patients needing single-lung ventilation, and may be better than VCV in respiratory disease patients 18.

In the postoperative period of cardiac surgeries, both controls had comparable effects in patients with preserved or depressed cardiac function, but PCV patients showed higher cardiac index values, decreased SVR and lower inspiratory pressure values, as compared to VCV patients 19.

PCV has been used in ICU to treat patients with severe respiratory diseases, with better results on oxygenation and better prevention of pulmonary tissue injury 20. These patients, already with cardiovascular and/or respiratory disorders, when submitted to procedures requiring CPP, are more difficult to have their ventilation controlled and normocapnia and oxygenation maintained. There are situations needing surgeries with pneumoperitoneum in patients already using PCV or when this modality is the best indication.

A major PCV characteristic is the dependence among patient's respiratory mechanics, inspiratory flow and volume. PCV prevents high pressures, determining the mechanism of pulmonary injury in the presence of differences in alveolar resistance and compliance, by maintaining airway pressure constant 21.

Maximum absorption is seen with relatively low pressures of 10 mmHg. Absorbed gas is eliminated by the lungs, sometimes even in the postoperative period, since volumes of more than 120 liters may be stored in our body. Bones are major reservoirs 22.

In pressure controlled ventilation there has been the need to increase tidal volume after pneumoperitoneum.

Peak inspiratory pressure is the maximum generated pressure to inflate lungs. It depends on the respiratory system elastic and resistive properties. Elastic components generate the pressure needed to change pulmonary volume while resistive properties represent the necessary pressure to generate gas flow 16.

There has been a proportional Paw Peak increase during CPP, without significant difference between VC and PC control modes.

CPP has determined proportional Paw plat increase, which has returned to baseline values after removal, without significant difference between volumes controlled and pressure controlled ventilation.

End tidal CO2 measured by capnometry was controlled by our study. To maintain PETCO2 within desired limits, volume was adjusted for VC group and inspiratory pressure was adjusted for PC group.

It has been observed that during prolonged CO2 abdominal inflation, peritoneal absorption leads to increase in blood concentration and elimination. The pattern is characterized by an early phase with fast increase in CO2 elimination (27-37 mL.min-1) soon after beginning of inflation, followed by a slower phase due to peritoneal surface distention with compression of peritoneal vessels 23. This two-phase pulmonary elimination pattern was also observed in animal models 24.

CO2 is highly soluble in blood generating an acid solution. To prevent hypercapnia and respiratory acidosis, ventilation should be increased in approximately 20% to 30% 15,22.

During CPP, PETCO2 is progressively increased with time, reaching its peak 40 minutes later, if ventilation is maintained constant 25, reaching a balance between CO2 absorbed by the abdominal cavity and that removed by ventilation. After this period there is storage in body reservoirs 22.

PETCO2 monitoring is critical during laparoscopic surgeries. In some situations, especially in the presence of respiratory diseases, PETCO2 measure may not be correlated to that of PaCO2, due to the presence of pulmonary shunt, increased IAP and anesthesia-induced changes. In such situations, there may be minor PETCO2 increase and major PaCO2 increase, with increased arterial-alveolar gradient (a-PET (PCO2)). Monitoring with blood gases analysis is recommended for patients with pulmonary disease.

Several studies indicate that the difference a-PET(PCO2) tends to increase or to become unforeseeable during CPP, especially in patients and animals with pulmonary dysfunction.

In ARDS patients, with changes in pulmonary compliance and resistance, a better respiratory pattern was observed with PCV 17.

Although PCV has been comparatively studied in the presence of pulmonary diseases, no comparative study was found on PCV and VCV in anesthesia with pneumoperi- toneum, where pulmonary compliance and resistance are changed, even if reversible at the end of surgery.

Several studies have shown that heart rate is not significantly changed during pneumoperitoneum 32-41.

Heart rate increase was similar for both groups after CPP without differences between volume controlled or pressure controlled ventilation.

Most studies report increased mean blood pressure (MBP) after abdominal cavity inflation for pneumoperitoneum 33-49.

Some studies have observed increased plasma concentration of antidiuretic hormone (ADH) after pneumoperitoneum 40,50,51, enough to determine increased MBP and SVR by vasoconstriction 40,52,53.

CO2 pneumoperitoneum leads to increased rennin 54-56, aldosterone 55 and norepinephrine plasma concentration. A study has not observed significant epinephrine and norepinephrine concentrations, and plasma rennin activity changes which could be related to increased MBP 40. Hypercapnia may increase MBP 1,57. In our study, PaCO2 values were within normality ranges, which may have contributed to MBP values.

There was no difference in mean blood pressure behavior between VC and PC groups, although VC group values were higher as compared to PC group since the beginning of the experiment, however within normality ranges.

Several studies have reported increased right atrium pressure during pneumoperitoneum 37,41,49,58,59.

During CPP, the mechanical inflation effect compresses capacitance vessels (venous system) and resistance vessels (arterial system) leading to significant increase in filling pressures in both left and right chambers 34,60,61.

IAP increase leads to intra-thoracic pressure increase with consequent pressure increase in cardiac chambers, with increased right atrium pressure and pulmonary capillary wedge pressure 28,62.

IAP increase has a two-phase effect on venous return, with increased compression of intra-abdominal capacitance vessels, followed by the impedance of abdominal venous return to lower limbs. During CPP, there is increased femoral veins pressure with decreased blood flow coming from lower limbs 63.

Other studies with swine 57 and dogs 35,64 have not observed changes in right atrium pressure during pneumoperitoneum.

Volume or pressure controlled ventilation has not interfered with right atrium pressure. In all moments, PC group values were lower as compared to VC group, maybe due to a possible characteristic of the group of animals. In M4 the difference was significant, however values were within normal ranges.

In a group of 16 patients physical status ASA I and II, there has been moderate respiratory acidosis 24 minutes after CO2 inflation 33, which might have been partially caused by decreased cardiac output, which decreases peripheral perfusion, which may be worsened by the attempt to increase ventilation, which increase cardiac output depression, worsening acidosis. CPP may have to be interrupted after several attempts to correct acidosis with increased ventilation 26.

A study on ventilatory effects, blood gases changes and oxygen consumption during laparoscopic hysterectomies has observed the development of metabolic acidosis during laparoscopy, but after the procedure major acidosis was respiratory acidosis 7.

Statistical analysis of arterial pH has shown interaction between groups and moments, with different profiles. Although higher variation in VC group values, there were no differences between groups in each moment. VC group had decreased values as from M1, being M1 > (M2 = M3 = M4). PC group had decreased values as from M1, being M1 > M2 e (M3 = M4) with intermediate values. Although the higher stability of arterial pH values during pressure controlled ventilation, there were no statistically significant differences between groups.

PETCO2 in expired air was a target of attention in this study. Tidal volume (VC group) and inspiratory pressure (PC group) were adjusted to maintain PETCO2 within desired ranges.

CO2 inflated in the abdominal cavity leads to hypercabia and acidosis and should be removed by increased ventilation, adjusting minute volume 65.

Ventilation adjustments, which affect PETCO2 values, promote PaCO2 changes.

Even with normal perioperative ventilation, there may be respiratory acidosis and hypercapnia up to one hour after CPP removal, due to built-up CO2 33,66.

In normal conditions, the difference between PaCO2 and PETCO2 (a -PET P(CO2)) is 2 to 5 mmHg 67,68.

Although there are many factors influencing a-PETP(CO2) gradient, it is considered a dead space index.

A study with swine submitted to CPP has observed increased dead space with consequent alveolar ventilation decrease and PaCO2 increase, if minute volume is not corrected 24.

In our study, a-PETP(CO2) gradient, measured in mmHg, in VC group was 4.0 in M1, 4.7 in M2, 7.2 in M3 and 5.2 in M4, while in PC group it was 5.1 in M1, 3.6 in M2, 5.2 in M3 and 4.3 in M4. These values show a lower alveolar-arterial gradient for pressure-controlled ventilation.

Several studies indicate that alveolar-arterial difference tends to increase with CPP time, becoming unforeseeable for prolonged procedures, especially in patients with pulmonary disease, and blood gases analysis is recommended for a better evaluation of arterial pCO2 26,27,30,31. Other studies point to helium as an alternative for promoting lower variations in alveolar-arterial difference, thus preventing hypercapnia 24,27,69.

CO2 volume stored during the procedure may lead to hypercapnia and respiratory acidosis in the postoperative period of patients with hypoventilation or decreased cardiac output, as well as in patients with pulmonary or cardiac disease.

In our study, PaCO2 variations were the same observed in PETCO2 with regard to groups and moments, even if with different magnitudes. There have been higher PaCO2 variations in the VC group, which has increased as a function of IAP, increase and presented statistically significant differences in M2. Ventilation controls (volume or pressure) affected PaCO2 with more linearity for pressure-controlled ventilation.

CPP increases dead space and may decrease alveolar ventilation if there is no ventilation control adjustment, especially in the presence of cardiac and pulmonary disease and with low FiO2 (oxygen inspiratory fraction) values.

Pulmonary compression with decreased compliance and increased airway pressure may lead to barotrauma and pneumothorax, to the inadequate distribution of ventilation with changes in ventilation / perfusion ratio, and to atelectasis. In spite of these changes, oxygenation may suffer major impairment 70.

Other studies have shown that PaO2 is not changed during CPP in adults 7,15,27.

In our study, volume and pressure controlled ventilation have not affected arterial pO2.

In the conditions of our study, volume controlled and pressure controlled ventilation had not determined significant hemodynamic changes.

Pressure controlled ventilation has determined higher PETCO2 and PaCO2 stability, as well as less variations in arterial pH.

Pressure controlled ventilation (PCV) was adequate to anesthetize dogs submitted to CO2 pneumoperitoneum, being necessary a strict ventilation control according to intra-abdominal pressure variations.



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Correspondence to
Dr. Antonio Roberto Carraretto
Address: Rua Cel. Monjardim, 289/1501
ZIP: 29015-500 City: Vitória, ES

Submitted for publication March 8, 2005
Accepted for publication September 8, 2005



* Received from Laboratório Experimental do CET/SBA do Departamento de Anestesiologia da Faculdade de Medicina de Botucatu (FMB UNESP), para o Programa de Pós-Graduação em Anestesiologia, Mestrado

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