Laparoscopic cholecystectomy has become an established surgical approach for symptomatic gallbladder disease because of its minimally invasive nature and favorable postoperative recovery profile. Compared with open surgery, laparoscopy is associated with smaller incisions, reduced postoperative pain, shorter hospitalization, earlier mobilization, and improved cosmetic outcomes. Nevertheless, laparoscopic surgery produces physiological alterations requiring careful anesthetic management. Creation of pneumoperitoneum, changes in patient positioning, and systemic absorption of insufflated carbon dioxide (CO₂) can influence cardiovascular function, respiratory mechanics, and acid–base homeostasis. These effects may be especially important in patients with limited cardiopulmonary reserve. Atkinson et al. highlighted the cardiovascular and ventilatory consequences of laparoscopic surgery [1]. Carbon dioxide is the preferred insufflation gas because it is nonflammable, readily available, highly soluble in blood, and rapidly eliminated through pulmonary ventilation. Nevertheless, intraperitoneal insufflation produces mechanical and biochemical changes. Elevation of intra-abdominal pressure compresses abdominal vascular structures, alters venous return, and increases systemic vascular resistance. Simultaneously, absorption of CO₂ across the peritoneal surface increases the systemic carbon dioxide load, potentially resulting in hypercapnia and respiratory acidosis. Gutt et al. described circulatory and respiratory complications associated with CO₂ insufflation and the roles of intra-abdominal pressure, insufflation duration, and underlying cardiopulmonary condition [2]. The cardiovascular response to pneumoperitoneum depends on the interaction between preload, afterload, myocardial contractility, autonomic activity, and circulating vasoactive substances. Initially, increased intra-abdominal pressure may displace blood from the splanchnic circulation into the central circulation, temporarily augmenting venous return. Further pressure increases can compress the inferior vena cava, restrict venous return, and reduce cardiac output. Increased systemic vascular resistance may simultaneously elevate arterial blood pressure despite reduced cardiac output. These changes are relevant during laparoscopic cholecystectomy, where pneumoperitoneum is combined with reverse Trendelenburg positioning. Joris et al. demonstrated increased mean arterial pressure and systemic vascular resistance with reduced cardiac index during laparoscopic cholecystectomy [3]. Heart rate and arterial blood pressure are commonly monitored indicators of cardiovascular response during laparoscopic surgery. Pneumoperitoneum may produce tachycardia through sympathetic stimulation, hypercapnia, and increased circulating catecholamines. Conversely, sudden peritoneal stretching can provoke vagally mediated bradycardia. These opposing responses illustrate the importance of monitoring throughout the procedure rather than relying on isolated measurements. Wittgen et al. documented hemodynamic and ventilatory changes associated with abdominal insufflation [4]. The magnitude of cardiovascular alterations is influenced by intra-abdominal pressure. Higher insufflation pressures may produce greater vascular compression, increased afterload, and more pronounced disturbances in cardiac output. Although moderate pneumoperitoneum is generally tolerated by healthy individuals, patients with hypovolemia, cardiovascular disease, or impaired compensatory mechanisms may experience clinically important instability. O’Malley and Cunningham described the combined effects of increased intra-abdominal pressure, patient positioning, and anesthetic management on cardiovascular and respiratory function [5]. Pneumoperitoneum also influences pulmonary mechanics. Elevated intra-abdominal pressure displaces the diaphragm cephalad, decreases functional residual capacity, reduces pulmonary compliance, and increases airway pressures. These changes may impair alveolar ventilation and contribute to ventilation–perfusion mismatch. General anesthesia independently reduces functional residual capacity and promotes atelectasis. Rauh et al. demonstrated that pneumoperitoneum and patient positioning both alter respiratory system compliance [6]. Following intraperitoneal insufflation, CO₂ diffuses across the peritoneal membrane into the circulation, increasing the carbon dioxide load requiring pulmonary elimination. If alveolar ventilation does not compensate, arterial carbon dioxide tension (PaCO₂) increases and arterial pH decreases. End-tidal carbon dioxide (ETCO₂) monitoring provides continuous, noninvasive assessment of exhaled CO₂ and guides ventilation. However, ETCO₂ may not accurately represent PaCO₂ when pulmonary perfusion or physiological dead space changes. Iwasaka et al. reported changes in pulmonary compliance, arterial carbon dioxide tension, and acid–base balance during and after laparoscopic cholecystectomy [7]. Arterial blood gas analysis provides additional information regarding the consequences of CO₂ insufflation. Arterial pH, PaCO₂, and bicarbonate (HCO₃⁻) characterize acid–base changes not fully assessed by capnography. The extent of alteration depends on absorbed CO₂, duration of pneumoperitoneum, ventilation strategy, and baseline respiratory function. Bardoczky et al. demonstrated measurable changes in respiratory mechanics following abdominal insufflation using continuous spirometry [8]. Hypercapnia may stimulate sympathetic activity and contribute to increased heart rate, arterial pressure, and myocardial workload. Elevated intra-abdominal pressure can also modify venous return and vascular resistance independently of CO₂ absorption. Galizia et al. compared hemodynamic and pulmonary changes during open cholecystectomy, CO₂ pneumoperitoneum, and abdominal wall-lifting cholecystectomy, demonstrating the influence of surgical approach on perioperative physiology [9]. Timing of measurements is important: hemodynamic responses may occur shortly after insufflation, while carbon dioxide absorption and acid–base changes evolve during surgery. Serial observations before insufflation, during pneumoperitoneum, and after desufflation characterize these patterns. Westerband et al. reported changes in cardiac index, mean arterial pressure, and peripheral vascular resistance during laparoscopic cholecystectomy [10]. The present study evaluated pulse rate, systolic and diastolic blood pressure, peripheral oxygen saturation (SpO₂), and ETCO₂ before, during, and after CO₂ pneumoperitoneum. Its secondary objective was to compare arterial pH, PaCO₂, and HCO₃⁻ before insufflation and after desufflation.

Study design and setting This prospective observational study, described in the dissertation as prospective cross-sectional, was conducted in the Department of Anaesthesiology, Jubilee Mission Medical College and Research Institute, Thrissur, Kerala, India, between November 2022 and June 2024. It evaluated hemodynamic and arterial blood gas changes during elective laparoscopic cholecystectomy under general anesthesia. Ethical considerations Institutional Ethics Committee approval was obtained (Reference No. 62/22/IEC/JMMC&RI). Written informed consent was obtained from participants after explanation of the study protocol. Preanesthetic evaluation included assessment of comorbidities and relevant laboratory investigations. Sample size The minimum required sample size was calculated using mean and standard deviation estimates from an earlier study of preinsufflation and postdesufflation arterial blood gas analysis in laparoscopic surgery. With a 95% confidence level and 80% statistical power, the estimated minimum sample size was 100 patients; 100 patients were included. Eligibility criteria Patients aged 21–55 years, weighing 40–80 kg, with American Society of Anesthesiologists (ASA) physical status I or II and scheduled for elective laparoscopic cholecystectomy lasting 60–135 minutes were eligible. Exclusions included ASA III or IV, uncontrolled diabetes or hypertension, cardiac or renal disorders, body mass index greater than 40 kg/m², coagulopathy, alcohol dependence, pregnancy, lactation, refusal of consent, or conversion to open cholecystectomy. Preoperative preparation and anesthetic management Preanesthetic assessment was performed the day before surgery. Patients were advised overnight fasting and received oral pantoprazole 40 mg and alprazolam 0.25 mg. The anesthesia workstation and airway equipment were checked. An 18-gauge intravenous cannula was placed in the right forearm and Ringer’s lactate infusion commenced. Monitoring included electrocardiography, noninvasive blood pressure, pulse oximetry, and capnography. Intravenous glycopyrrolate 0.004 mg/kg and ondansetron 0.1 mg/kg were administered. After three minutes of preoxygenation with 100% oxygen, anesthesia was induced using propofol 2 mg/kg. Endotracheal intubation followed vecuronium 0.1 mg/kg. Anesthesia was maintained with 50% nitrous oxide in oxygen and either isoflurane or sevoflurane, with additional vecuronium as required. Pneumoperitoneum and ventilation Carbon dioxide pneumoperitoneum was established with intra-abdominal pressure maintained at 12–15 mmHg and insufflation flow at 5–10 L/min. Controlled ventilation used tidal volumes of 8–10 mL/kg and respiratory rates of 12–16 breaths/minute. Peak airway pressure was maintained below 35 cmH₂O. Intravenous paracetamol 1 g was administered for analgesia. Hemodynamic monitoring Pulse rate, systolic and diastolic blood pressure, SpO₂, and ETCO₂ were recorded before insufflation, at predetermined intervals after CO₂ insufflation, and after desufflation. The results document observations at 5, 10, 15, 20, 25, 30, 40, 50, and 60 minutes. Measurements were recorded in the study proforma. Arterial blood gas analysis Arterial blood was collected five minutes before insufflation and five minutes after desufflation. At each time point, 2 mL was collected anaerobically in a preheparinized syringe for measurement of pH, PaCO₂, and HCO₃⁻. Recovery from anesthesia At completion of surgery, residual neuromuscular blockade was reversed with intravenous neostigmine 0.05 mg/kg and glycopyrrolate. Patients were extubated after adequate recovery of muscle power, protective reflexes, and tidal volume. Outcome measures Primary outcomes were serial changes in pulse rate, blood pressure, SpO₂, and ETCO₂. Secondary outcomes were changes in arterial pH, PaCO₂, and HCO₃⁻ between preinsufflation and postdesufflation. Statistical analysis Data were entered into Microsoft Excel and analyzed using IBM SPSS Statistics version 25. The dissertation describes analysis of variance for quantitative variables and chi-square testing for categorical variables, with p<0.05 considered significant. Reported test statistics and p-values were retained from the original dissertation.

A total of 100 patients undergoing laparoscopic cholecystectomy under general anesthesia were evaluated. Hemodynamic parameters were assessed serially before, during, and after pneumoperitoneum, and arterial blood gas parameters were compared between preinsufflation and postdesufflation measurements. Demographic characteristics Of 100 participants, 41 (41%) were aged 21–30 years, 32 (32%) were aged 31–40 years, and 27 (27%) were aged 41–50 years. Women constituted 81% of the cohort and men 19%. Table 1. Demographic characteristics of the study population (N = 100) Characteristic Number (n) Percentage (%) Age 21–30 years 41 41.0 Age 31–40 years 32 32.0 Age 41–50 years 27 27.0 Male 19 19.0 Female 81 81.0 Total 100 100.0 Pulse rate and blood pressure Mean pulse rate increased from 74.16 ± 5.63 beats/min before insufflation to 89.96 ± 7.04 at five minutes (p<0.001), reaching 93.71 ± 7.10 at 15 minutes (p<0.001). It subsequently declined to 74.09 ± 5.21 at 60 minutes (p=0.9274) and 73.54 ± 4.57 after desufflation (p=0.288). Systolic blood pressure increased from 115.53 ± 8.54 mmHg to 132.11 ± 7.37 at five minutes and peaked at 138.42 ± 7.96 at 10 minutes (p<0.001). At 60 minutes it was 116.76 ± 6.04 (p=0.241); postdesufflation it was 118.01 ± 5.75 (p=0.001). Diastolic blood pressure increased from 74.18 ± 5.87 to 92.17 ± 6.19 at five minutes and peaked at 96.48 ± 6.84 at 10 minutes (p<0.001). At 60 minutes it was 75.61 ± 7.64 (p=0.1391), and postdesufflation 74.09 ± 5.63 (p=0.912). Table 2. Changes in pulse rate, systolic blood pressure, and diastolic blood pressure (mean ± SD) Interval Pulse (beats/min) SBP (mmHg) DBP (mmHg) Preinsufflation 74.16 ± 5.63 115.53 ± 8.54 74.18 ± 5.87 5 min 89.96 ± 7.04 132.11 ± 7.37 92.17 ± 6.19 10 min 91.97 ± 10.97 138.42 ± 7.96 96.48 ± 6.84 15 min 93.71 ± 7.10 137.91 ± 9.18 95.56 ± 6.88 20 min 89.16 ± 7.13 132.56 ± 8.52 89.48 ± 8.12 25 min 85.19 ± 7.13 129.06 ± 7.69 86.16 ± 6.36 30 min 81.68 ± 7.42 125.91 ± 6.24 80.96 ± 9.71 40 min 78.27 ± 7.61 122.23 ± 5.77 78.27 ± 7.61 50 min 76.20 ± 5.55 119.59 ± 5.96 75.49 ± 7.04 60 min 74.09 ± 5.21 116.76 ± 6.04 75.61 ± 7.64 Postdesufflation 73.54 ± 4.57 118.01 ± 5.75 74.09 ± 5.63 Compared with baseline, all three parameters were reported significant at 5–40 minutes (p<0.001). At 50 minutes, reported p-values were 0.0106, <0.001, and <0.001 for pulse rate, SBP, and DBP, respectively. At 60 minutes the corresponding p-values were 0.9274, 0.241, and 0.1391; after desufflation they were 0.288, 0.001, and 0.912. Oxygen saturation and end-tidal carbon dioxide Peripheral oxygen saturation remained stable, with mean SpO₂ values approximately 99.80%–99.94% and no statistically significant variation (p>0.05). ETCO₂ rose from 29.54 ± 1.76 mmHg at baseline to 32.53 ± 1.71 at five minutes and 34.46 ± 1.40 at 10 minutes (both p<0.001). It peaked at 34.74 ± 1.32 at 15 minutes, then decreased to 30.76 ± 0.95 at 60 minutes. After desufflation, ETCO₂ was 31.58 ± 6.94 mmHg (p=0.007). Table 3. End-tidal carbon dioxide changes during pneumoperitoneum Interval ETCO₂ (mmHg), mean ± SD t-value p-value Preinsufflation 29.54 ± 1.755 — — 5 min 32.53 ± 1.708 19.490 <0.001 10 min 34.46 ± 1.396 28.199 <0.001 15 min 34.74 ± 1.323 23.715 <0.001 20 min 34.01 ± 1.839 17.994 <0.001 25 min 33.63 ± 1.862 16.529 <0.001 30 min 32.80 ± 1.758 14.153 <0.001 40 min 32.14 ± 4.070 5.869 <0.001 50 min 31.25 ± 1.300 7.835 <0.001 60 min 30.76 ± 0.950 6.107 <0.001 Postdesufflation 31.58 ± 6.940 2.745 0.007 Arterial blood gas parameters Mean arterial pH decreased from 7.40 ± 0.031 before insufflation to 7.35 ± 0.029 after desufflation (t=12.4; p<0.001). PaCO₂ increased from 37.00 ± 0.82 to 39.53 ± 1.11 mmHg (t=18.02; p<0.001), while HCO₃⁻ increased from 22.60 ± 0.60 to 23.40 ± 0.62 mmol/L (t=9.419; p<0.001). Table 4. Arterial blood gas parameters before insufflation and after desufflation Parameter Preinsufflation, mean ± SD Postdesufflation, mean ± SD t-value p-value pH 7.40 ± 0.031 7.35 ± 0.029 12.400 <0.001 PaCO₂ (mmHg) 37.00 ± 0.82 39.53 ± 1.11 18.020 <0.001 HCO₃⁻ (mmol/L) 22.60 ± 0.60 23.40 ± 0.62 9.419 <0.001 Overall, CO₂ pneumoperitoneum was associated with early increases in pulse rate and blood pressure, with peak systolic and diastolic pressures at 10 minutes and peak pulse rate and ETCO₂ at 15 minutes. Most hemodynamic parameters approached baseline over time. Oxygen saturation remained stable. Arterial blood gas analysis demonstrated decreased pH and increased PaCO₂ and HCO₃⁻ after desufflation.

The present prospective observational study evaluated hemodynamic and arterial blood gas changes associated with carbon dioxide pneumoperitoneum in 100 patients undergoing laparoscopic cholecystectomy under general anesthesia. Significant changes occurred in pulse rate, systolic and diastolic blood pressure, ETCO₂, and arterial blood gas parameters. The most pronounced cardiovascular responses occurred within 10–15 minutes after insufflation, followed by progressive stabilization. Peripheral oxygen saturation remained stable. These observations indicate measurable cardiovascular and respiratory responses even in ASA I and II patients. The study population comprised 81% women, with 41% aged 21–30 years. This predominance may reflect the patient distribution at the institution. However, the study was not designed to compare physiological responses by sex or age, and these demographic characteristics cannot independently explain the hemodynamic changes. Mean pulse rate increased from 74.16 ± 5.63 beats/min before insufflation to 89.96 ± 7.04 at five minutes and peaked at 93.71 ± 7.10 at 15 minutes. It subsequently declined toward baseline. Early tachycardia may reflect sympathetic activation associated with elevated intra-abdominal pressure, peritoneal stretching, and systemic CO₂ absorption. Meftahuzzaman et al. reported increased pulse rate and blood pressure following insufflation and positioning [11]. Differences in timing may relate to insufflation pressure, anesthesia, and patient characteristics. Umar et al. examined different intra-abdominal pressures and reported heart-rate increases during CO₂ insufflation with reductions after desufflation [12]. Mean systolic pressure increased from 115.53 ± 8.54 mmHg to 138.42 ± 7.96 at 10 minutes, while mean diastolic pressure rose from 74.18 ± 5.87 to 96.48 ± 6.84 mmHg. Both subsequently declined. Increased systemic vascular resistance from elevated intra-abdominal pressure, vascular compression, and neurohumoral activation may explain this response. Yeo et al. found that anesthetic management influenced the blood-pressure response and that PaCO₂ elevation alone did not necessarily explain hypertension during insufflation [13]. Joris et al. demonstrated increased mean arterial pressure and systemic vascular resistance alongside reduced cardiac index [3]. Cardiac output and vascular resistance were not directly measured in the present study, so mechanistic explanations remain inferential. Peripheral oxygen saturation remained approximately 99.80%–99.94%, suggesting oxygenation was maintained during controlled ventilation. However, stable saturation does not exclude altered pulmonary compliance or ventilation–perfusion relationships. ETCO₂ increased from 29.54 ± 1.76 mmHg to 34.74 ± 1.32 at 15 minutes, then declined while remaining elevated after desufflation. Increased CO₂ absorption from the peritoneal cavity adds to the pulmonary elimination requirement. Makwana et al. reported increased ETCO₂ after insufflation and reduction toward baseline after desufflation [14]. Iwasaka et al. described altered respiratory mechanics and arterial CO₂ tension during laparoscopic cholecystectomy [7]. Reduced compliance and increased airway pressure may contribute to impaired CO₂ elimination despite maintained oxygen saturation. Arterial pH decreased from 7.40 ± 0.031 to 7.35 ± 0.029, PaCO₂ increased from 37.00 ± 0.82 to 39.53 ± 1.11 mmHg, and bicarbonate increased from 22.60 ± 0.60 to 23.40 ± 0.62 mmol/L. The reduction in pH accompanying increased PaCO₂ is compatible with respiratory effects of systemic CO₂ absorption. Although statistically significant, the mean values remained within or near conventional physiological reference ranges. Shobhana et al. described pH changes between preinsufflation and postdesufflation arterial samples [15]. Hakeem et al. reported changes in PaCO₂, pH, ETCO₂, and bicarbonate during laparoscopic cholecystectomy [16]. Mutetwa et al. reported increased PaCO₂ and reduced pH during pneumoperitoneum under low tidal volume ventilation [17]. These findings emphasize continuous cardiovascular and capnographic monitoring, particularly during the first 10–15 minutes after insufflation. Recognition of early changes can guide clinical adjustments in anesthetic depth, ventilation, and intra-abdominal pressure when indicated. Capnography provides continuous information, whereas arterial blood gas analysis may be useful when accurate PaCO₂ and acid–base assessment is required. Westerband et al. demonstrated increased peripheral resistance and reduced cardiac index during laparoscopic cholecystectomy [10], emphasizing that stable arterial pressure does not necessarily imply unchanged cardiovascular performance. The principal strength of the study was serial cardiovascular and respiratory assessment before, during, and after pneumoperitoneum, combined with arterial blood gas measurements. Limitations include single-center design, restriction to ASA I and II patients, lack of cardiac output and vascular resistance measurements, and arterial blood gas sampling only before insufflation and after desufflation. Without an unexposed comparison group, independent effects of CO₂ insufflation cannot be fully separated from anesthesia, positioning, or surgical stimulation. The original reported statistical tests also require confirmation against patient-level data.

Carbon dioxide pneumoperitoneum during laparoscopic cholecystectomy under general anesthesia was associated with significant changes in cardiovascular parameters, end-tidal carbon dioxide, and arterial blood gas values. Pulse rate and arterial blood pressure increased during the early period after insufflation, with peak changes within 10–15 minutes and subsequent stabilization. End-tidal carbon dioxide increased significantly, while peripheral oxygen saturation remained stable. Arterial blood gas analysis demonstrated reduced pH and increased PaCO₂ and bicarbonate following desufflation. These findings support vigilant hemodynamic and respiratory monitoring, particularly during the initial period after CO₂ insufflation.

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