Cardiorespiratory and blood gas alterations during laparoscopic surgery for intra-uterine artificial insemination in dogs

Abstract

Cardiorespiratory and blood gas alterations were evaluated in 6 healthy dogs that underwent a laparoscopic procedure using isoflurane anesthesia and carbon dioxide (CO₂) pneumoperitoneum for 30 min. Heart rate, respiratory rate, body temperature, venous blood pH, partial pressure of CO₂ and oxygen, oxygen saturation, total carbon dioxide (TCO₂) and bicarbonate were monitored. Significant alterations were hypercapnia, hypoventilation, and respiratory acidosis.

During laparoscopy, pneumoperitoneum is essential to provide a surgical field, allowing visibility and performance of surgical maneuvers (1). Carbon dioxide (CO₂) is the most commonly used gas for pneumoperitoneum. After its introduction into the peritoneal cavity, CO₂ diffuses throughout the tissues and becomes balanced in all body compartments (2). Minimally invasive procedures, however, can cause cardiocirculatory and respiratory alterations due to hypertensive pneumoperitoneum, hypercapnia, and patient positioning.

The intra-abdominal pressure in the dog should not be greater than 10 to 12 mmHg (3) or increases in arterial blood pressure, pulmonary vascular resistance, total peripheral resistance, and a decrease in cardiac output may occur (4). Hypercarbia may occur due to local CO₂ absorption by the peritoneum and ventilatory restriction caused by abdominal distension. Hemodynamic alterations can be caused by the direct effect of CO₂ on the cardiovascular system and indirectly through sympathetic stimulation. Tachycardia, arterial hypertension, and arrhythmias may also be observed (4).

This study evaluated cardiorespiratory alterations, venous blood gas alterations, and body temperature during pneumoperitoneum in bitches submitted to laparoscopy for intra-uterine artificial insemination. Six healthy mixed-breed adult bitches weighing 6 to 17 kg were used. Heart rate (HR), respiratory rate (RR), and body temperature (BT) were measured. pH, partial pressure of carbon dioxide (PCO₂), partial pressure of oxygen (PO₂), oxygen saturation (SatO₂), total carbon dioxide (TCO₂), and bicarbonate (HCO₃⁻) were analyzed using venous blood collected from the jugular vein.

The animals were pre-medicated with acepromazine (Acepran; Univet, Campinas, Brazil), 0.05 mg/kg body weight (BW), IM, and pethidine (Dolosal; Cristália, Brazil), 3.0 mg/kg BW, IM. Anesthesia was induced with 1% propofol (Fresofol; Fresenius Kabi, Brazil), 5.0 mg/kg, IV, followed by orotracheal intubation and maintenance with isoflurane (Isothane; Baxter, Brazil) in a semi-closed circuit and spontaneous breathing. The animals were maintained in surgical anesthetic plane, which was controlled through clinical evaluation each 5 min; ocular and podal reflexes, jaw muscular tone and respiratory rate were monitored. Average isoflurane concentration was 2%. Pneumoperitoneum was created through a flux of 0.5 to 1.0 L of CO₂/min to produce an intra-abdominal pressure of 8 to 10 mmHg (3). For the blood gas analysis (I-Stat Precision — EG-7; Abbott Laboratories, New Jersey, USA), 0.5-mL blood samples were collected before any anesthetic pre-medication (T₀), after anesthesia was established (T₁), after abdominal insufflation (T₂), within 15 and 30 min (T₃ and T₄) of pneumoperitoneum, and 15 and 30 min (T₅ and T₆) after abdominal deflation. During the experimental period, laparoscopic artificial insemination was performed, a simple procedure that lasted approximately 15 min.

The study herein was conducted according to a randomized complete block design, and variables were subjected to Kolmorogov-Smirnov and Lilliefors normality tests. Blood HCO₃⁻ was analyzed with the Student Newman-Keuls (SNK) test. The non-normal variables (HR, RR, BT, pH, PCO₂, TCO₂, PO₂, SatO₂) had their normality and homoscedasticity adjusted by logarithmic transformation and were analyzed by the SNK test (PCO₂, SatO₂, and PO₂). The non-parametric variables (HR, RR, BT, pH, and TCO₂) were analyzed by the Kruskal-Wallis test.

Significant cardio-respiratory changes were detected during laparoscopy in the anesthetized dogs (Table 1). The values (mean + standard deviation) for TCO₂ and HCO₃⁻ ranged from 24.8 ± 1.8 to 27.7 ± 2.7 and 23.5 ± 1.5 to 25.4 ± 2.0, respectively. There were no significant differences among T₀ to T₆ for TCO₂ and HCO₃. The observed changes may relate in part to general anesthesia, CO₂ gas insufflation and high intra-abdominal pressure.

Table 1.

Mean ± standard deviation of heart rate (HR), respiratory rate (RR), body temperature (BT), and venous blood gas results: partial pressure of CO₂ (PCO₂) and O₂ (PO₂), pH, and O₂ saturation (SatO₂) during CO₂ pneumoperitoneum between time intervals (T) in 6 healthy dogs

T	HR (bpm)	RR (brpm)	BT (°C)	PCO2 (mmHg)	PO2 (mmHg)	SatO2 (%)	pH
T0	105.3 ± 14.5a	56.5 ± 48.4a	38.4 ± 0.5a	41.9 ±6.6b	42.0 ± 5.3b	70.8 ± 10.5b	7.37 ± 0.05a
T1	109.3 ± 18.7a	12.0 ± 3.8a	36.5 ± 0.4a	45.6 ± 8.4b	113.3 ±25.1a	95.8 ± 3.8a	7.32 ± 0.06a
T2	103.3 ± 9.8a	8.8 ± 2.6a,b	35.8 ± 0.3a	60.0 ± 6.6a	211.8 ± 138.2a	96.5 ± 5.4a	7.23 ± 0.04b
T3	97.7 ± 17.1a	10.2 ± 3.4a,b	35.8 ± 1.4a	71.1 ± 19.4a	141.5 ± 82.2a	96.3 ± 3.0a	7.16 ± 0.09b
T4	93.2 ± 13.3a	12.3 ±5.4a	34.7 ± 0.4a,b	65.3 ± 23.2a	189.2 ± 147.6a	96.3 ± 3.9a	7.20 ± 0.10b
T5	112.3 ± 40.1a	30.0 ± 26.0a	34.6 ± 0.4a,b	49.1 ± 12.9b	130.7 ± 139.7a,b	77.0 ± 25.6a,b	7.31 ± 0.07a
T6	115.8 ± 35.4a	23.8 ±12.2a,c	34.9 ± 0.6a,b	43.9 ± 4.9b	40.0 ± 11.8b	73.3 ± 13.3a,b	7.34 ± 0.05a

T₀ — before anesthetic premedication was given, T₁ — time anesthesia was established, T₂ — immediately after abdominal insufflation, T₃ — within 15 min of pneumoperitoneum, T₄ — within 30 min of pneumoperitoneum, T₅ — 15 min after abdominal deflation. T₆ — 30 min after abdominal deflation. bpm — beats per min, brpm — breaths per min.

^a,b,cMeans with distinct superscripts within the column are significantly different (P < 0.05).

General anesthesia with isoflurane was used, as this is a safe choice that also allowed for administration of a high percentage of O₂. Laparoscopic surgery has been reported using sedatives and regional anesthesia. However it is not possible to guarantee airway protection and some degree of respiratory depression and hypercapnia occured in humans (4), although it was not observed in dogs (1). General anesthesia with orotracheal intubation guarantees a greater control of ventilation, allowing for compensation of CO₂ absorption that is induced by the pneumoperitoneum (4,5), and also results in adequate muscular relaxation and abdominal distention (4).

Gases such as CO₂, nitrous oxide (N₂O) (6), atmospheric air, oxygen (O₂), nitrogen (N₂), and helium (He) (7) can be used to produce pneumoperitoneum. Because CO₂ is very soluble in blood, it is promptly absorbed by the peritoneum, causing hypercapnia and acidosis (4,8). However, it is by far the most used gas during laparoscopic procedures (8).

Hypertensive pneumoperitoneum leads to cranial dislocation of the diaphragm, reducing lung volume and compliance and increasing airway resistance. This causes reduced alveolar ventilation and impairs matching of ventilation and perfusion with consequent hypercapnia worsened by the peritoneal absorption of CO₂, and by hypoxemia (4). The intra-abdominal pressure is of extreme importance to the physiopathology of hypercapnia, as it increases the absorption and reduces the elimination of CO₂ (4,9). The intra-abdominal pressure of 8 to 10 mmHg used in this study was low in comparison to the pressure referred to by others (10), but it allowed adequate visualization and manipulation of abdominal viscera. Additionally, there was a significant increase in PCO₂ during pneumoperitoneum, represented by T₂, T₃, and T₄ with a maximum value within 15 min during T₃. After abdominal deflation in T₅, PCO₂ returned to the normal value since CO₂ is highly soluble, allowing for a fast diffusion of the gas throughout the blood and body tissues and its elimination by the lungs (11). Partial pressure carbon dioxide increases could also relate to abdominal distention, promoted by pneumoperitoneum, which reduces CO₂ elimination by the lungs.

Acidosis was a consistent finding during abdominal insufflation with CO₂. When comparing the means of venous blood pH intra-operatively and during the recovery from the anesthetic, there were significant differences in T₂, T₃, and T₄ — the time when pneumoperitoneum was maintained. According to another study (9), discrete systemic acidosis is a clinically recognized side effect and acceptable during CO₂ pneumoperitoneum. The peritoneum allows CO₂ diffusion to tissues and absorption to the systemic circulation, leading to a decrease in plasma and peritoneal pH (9,12) through the liberation of hydrogen ions, according to the equation of CO₂ dissociation:

$${\text{H}}_2\text{O}+{\text{CO}}_2\leftrightarrow {\text{H}}_2{\text{CO}}_3\leftrightarrow {\text{H}}^{+}+{{\text{HCO}}_3}^{-}$$

Total carbon dioxide is a discrete variable that was within the normal range for this species. Total carbon dioxide represents both HCO₃⁻ and soluble CO₂ (13), and is impacted by changes in metabolic activity. Although the venous blood gas evaluations of PO₂ and SatO₂ did not reflect the lungs oxygenating capacity, we observed increased PO₂ and SatO₂ in the venous blood during oxygen supplementation. An increase in PCO₂ results in additional bicarbonate in extracellular fluid (4), and there was an increase in plasma bicarbonate during T₂, T₃, and T₄, which occurred concomitantly with the decrease in pH, but was not significant.

The renal response to an increase of H⁺ concentration in a patient takes several hours or even days (13). During the pneuroperitoneum, the absorbed CO₂ must be totally excreted by the lungs and hypercapnia must be controlled by maintaining adequate ventilation or an increase in tidal volume or rate. Other authors (4,9) have discussed the benefits of assisted or controlled ventilation as a method of preventing hypercapnia and respiratory acidosis during pneumoperitoneum. One must consider the consequences of hypercapnia and acidosis as compared with the increase in maximum respiratory and plateau pressures associated with intermittent positive pressure ventilation, which may cause pulmonary injury. Although positive-end expiratory pressure may improve gas exchange during pneumoperitoneum, this pressure, associated with the increased intra-abdominal pressure, increases intra-thoracic pressure reducing cardiac output. Considering the disadvantages of assisted ventilation, the present study was conducted using spontaneous breathing.

Tachycardia may occur as a compensatory response to decreased venous return (14), due to the increase in abdominal pressure or to the absorption of CO₂; however, in the present study, the alterations in HR were not significant. Anesthesia can significantly reduce compensatory responses to decreased venous return as others have shown in a model of hypovolemia in isoflurane anesthetized dogs (15).

The respiratory rate (RR) showed large individual variations. There was a significant difference in means between the basal value (T₀) compared with T₂ and T₃ as well as between T₂ and T₆. The decrease in RR observed in T₁, T₂, T₃, and T₄ may be related to the respiratory depression caused by the pre-anesthetic and anesthetic drugs (13). In this study, some tachypnea was expected in response to the hypercapnia or from the stimulus from increased abdominal pressure. However, the effect of the anesthetic agents on the central nervous system depresses the ventilatory response to CO₂, blocking the compensatory physiological effect (11).

The BT measurements showed a significant difference between the basal value (T₀) and T₄, T₅, and T₆, which shows a progressive reduction. Although, there was no statistically significant difference in T₁, T₂, and T₃, these values were below reference levels. Hypothermia during anesthesia was initiated at T₁, probably due to acepromazine’s effect on the body’s temperature control centre and on vasodilation (13). The gradual reduction in body temperature, after induction of anesthesia, may be caused by an association of several factors, such as the hypotensive effect of propofol and isoflurane with consequent vasodilation from isoflurane, cool gas inhalation, abdominal insufflation with CO₂, and the administration of intravenous fluids at room temperature.

Unfortunately this study did not document and standardize isoflurane percent as a means to ensure similar inhalant depressant effects among these dogs. Ideally, individual determinations of minimum alveolar concentration (MAC) preceeding this study could have enabled each dog to be stabilized at 1.2 MAC and thus be more likely to have similar respiratory and cardiovascular depression associated with isoflurane. The use of pre-medication could also result in varied responses among the dogs. The clinical approach used, however, may more closely relate to case management where premedication is used and anesthetic depth judged based on standard monitoring.

In conclusion, dogs undergoing pneumoperitoneum during a 30-minute period developed discrete hypercapnia, acidosis, and a compensatory elevation in blood bicarbonate. Hypothermia was also observed following premedication and worsened during the period of anesthesia. CVJ