One-lung ventilation (OLV) remains pivotal in a wide array of thoracic procedures that require isolation and collapse of the operative lung while maintaining ventilation in the contralateral, non-operative lung1,2 . This selective ventilation strategy confers dual advantages: it preserves a contaminant-free environment in the ventilated lung, protecting it from infection or haemorrhage, and it also grants the surgeon an unobstructed view of the operative field, thus facilitating technically intricate resections3. Despite these benefits, OLV introduces substantial physiologic intricacies, mainly arising from ventilation-perfusion (V/Q) mismatching in the lungs. As the non-ventilated lung is perfused but not ventilated, a significant intrapulmonary shunt develops, leading to marked hypoxemia if compensatory mechanisms fail. Among the body's adaptive responses, hypoxic pulmonary vasoconstriction (HPV) curtails blood flow to under-ventilated alveoli, thereby directing perfusion toward well-ventilated lung segments and partially compensating for the ventilation-perfusion mismatch 4. However, the effectiveness of HPV is modulated by multiple factors commonly encountered during general anaesthesia, including inhaled anaesthetics, intravenous agents, and fluctuations in arterial oxygen and carbon dioxide tensions5. In clinical practice, maintaining adequate oxygenation during OLV thus requires a finely tuned approach that addresses the complex interplay between alveolar ventilation, perfusion, and metabolic demands. One important emerging concept in this context is the deliberate elevation of arterial carbon dioxide tension (PaCO₂) within permissible limits, commonly referred to as permissive hypercarbia. While hypercarbia is traditionally avoided due to concerns about potential adverse effects—particularly on intracranial pressure and systemic haemodynamics—recent investigations propose that mild to moderate increases in PaCO₂ might enhance lung mechanics and improve oxygenation 6,7. The underlying mechanisms may include improved pulmonary vasoregulation, reduced alveolar dead space, and protective effects on the alveolar-capillary interface. Permissive hypercarbia can also attenuate inflammatory responses and mitigate ventilator-induced lung injury by allowing a lower tidal volume ventilation strategy8. Still, the clinical efficacy of permissive hypercarbia in the setting of OLV remains an area of active exploration. Some studies indicate improved arterial oxygenation and reduced incidence of alveolar collapse during OLV under mild hypercarbia. In contrast, others highlight potential risks such as increased sympathetic tone and compromised haemodynamics in susceptible patients9,10. Consequently, it is imperative to conduct well-designed, randomized controlled trials to elucidate whether permissive hypercarbia can be safely and reliably used to optimize oxygenation in patients undergoing thoracic surgeries. Against this background, the present study aims to compare arterial oxygenation, respiratory mechanics, and O₂ delivery under conditions of normocarbia versus permissive hypercarbia in patients undergoing OLV for thoracic surgical procedures. We hypothesize that permissive hypercarbia will significantly enhance arterial oxygenation without imposing substantial hemodynamic instability. Should this be confirmed, permissive hypercarbia may serve as a valuable clinical tool, improving oxygenation in scenarios where achieving optimal ventilation is inherently challenging.

Study Design and Approval This potential, randomized comparative study was performed inside the Department of Anaesthesiology at a tertiary level hospital, after obtaining approval from the Institutional Evaluation Board and Ethical Committee. The study is registered at clinicaltrials.gov (registration quantity: CTRI/2024/05/067338), and all strategies adhered to the announcement of Helsinki pointers. Written knowledgeable consent was acquired from each participant. Patient Selection A study of seventy-four patient’s (age ≥18 years) had been enrolled. All patient’s had been labelled as American Society of Anaesthesiologists (ASA) bodily popularity I or II and were scheduled for elective thoracic surgical treatment requiring one-lung ventilation. Exclusion criteria protected loss of knowledgeable consent, emergency surgeries, pre-present arrhythmias, coronary heart failure, obstructive or restrictive lung diseases, multiplied intracranial strain, and any liver or renal dysfunction . Randomization and Group Allocation Using a laptop-generated block randomization series (allocation ratio 1:1), patients were assigned into one among two groups, each containing 37 contributors: Group A (Normocarbia): PaCO₂ maintained within 38–42 mmHg for 30 minutes during OLV. Group B (Permissive Hypercarbia): PaCO₂ maintained within 45–50 mmHg for 30 minutes during OLV. The anaesthesiologist responsible for intraoperative management was blinded to the randomization. An independent observer recorded all data. Anaesthesia Protocol All patients underwent well-known anaesthesia induction. Continuous monitoring included electrocardiogram, pulse oximetry, invasive blood pressure, Bispectral index (BIS), and capnography. Induction was done with midazolam (0.01–0.5 mg kg-1), propofol (1.5–2 mg kg-1), fentanyl (3–4 μgkg-1), and rocuronium (0.9zero mg kg-1). After induction, a left-sided double-lumen endotracheal tube (35 or 37 Fr. for women, 37 or 39 Fr. for adult males) was placed under fibre-optic bronchoscope guidance. An arterial line was placed inside the radial artery of the non-dominant hand for non-stop invasive blood strain (IBP) measurement and arterial blood fuel (ABG) sampling. Internal jugular venous cannulation was done under local anaesthesia by ultrasound guidance for central venous pressure (CVP) management. Ventilatory Management After induction, both lungs were ventilated within the supine position with tidal volumes of 6–8 mL kg-1 of predicted frame weight, an I: E ratio of 1:2, and 5 cmH₂O positive end expiratory pressure (PEEP). The fraction of inspired oxygen (FiO₂) was set to 0.5 and adjusted to maintain oxygen saturation above 90%, and the respiratory rate was adjusted to hold a goal end-tidal CO₂ of 35–38 mmHg before randomization. Sevoflurane (1. 0 vol%) and incremental fentanyl infusions and muscle relaxants were used for the maintenance of anaesthesia, preserving BIS values between 40 and 60. Patients were then placed in lateral decubitus position. After re-confirming the position of the double lumen tube by fibre -optic bronchoscopy ,one-lung ventilation was initiated via clamping the non-based lumen of the double-lumen tube. As soon as OLV commenced, group A maintained normocarbia (38–42 mmHg) and group B was allowed a controlled elevation of PCO2 (45–50 mmHg) for 30 minutes. The primary endpoint was measurement of arterial oxygen partial pressure (PaO₂) via arterial blood gases in both the groups during OLV. Data Collection Key variables recorded included: 1. Respiratory parameters: tidal volume (TV), respiratory rate (RR), peak inspiratory pressure (PIP), plateau pressure (PPL), mean airway pressure (P mean), dynamic compliance (Cdyn), and static compliance (C stat). 2. Arterial blood gases (ABG): PaO₂, PaCO₂, pH, bicarbonate, lactate, and electrolytes. 3. Hemodynamic indices: invasive blood pressure (systolic, diastolic, mean), heart rate, CVP. 4.Oxygen delivery (DO₂) and arterial oxygen content (CaO₂) are calculated by standard formulas:CaO2=1.39×Hb×SaO2+0.0031×PaO2 5. DO2=CaO2×Cardiac Output Statistical Analysis All statistical analysis were performed using a software program (SPSS or equal). Continuous variables have been expressed as suggested ± widespread deviation (SD) and compared using student's t-test for impartial samples. Depending on the characteristics of the variables, either the chi-square test or Fisher's exact test was applied. A p-value < 0.05 was deemed statistically significant.

Seventy-four patients had been enrolled, with 37 in each group (Group A: Normocarbia, Group B: Permissive Hypercarbia(Figure 1).The demographic profile were similar, and did not have statistically sizeable differences between the groups (p > zero.05). (Table 1). The pre- operative pulmonary function tests(PFT) and parameters (FVC, FEV₁, and FEV₁/FVC ratio) were also statistically similar. In examining the primary endpoint—arterial oxygenation PaO₂ was significantly elevated in Group B compared to Group A (366.38 ± 117.28 mmHg vs. 295.46 ± 118.41 mmHg, p = 0.012) PaO₂/FiO₂ Ratio was also elevated in Group B (7.33 ± 2.35) compared to Group A (5.91 ± 2.37) significantly p value=0.012 (Table 2). We observed that permissive hypercarbia was associated with a marked and statistically significant improvement in oxygenation during one-lung ventilation (Figure 2). The increased PaO₂ in Group B suggests that mild elevation of PaCO₂ might augment pulmonary vasoregulation, possibly improving hypoxic pulmonary vasoconstriction or redistributing blood flow in a way that enhances V/Q matching. However CO2 and DO2 were higher in the Group B i..e Hypercarbia Group than the Normocarbia Group (Table 3),( Figure 3). Regarding ventilatory mechanics, maintaining normocarbia in Group A necessitated higher respiratory rates and manifested in modest increases in peak and mean airway pressures (Table 4). Conversely, Group B had lower ventilatory rates but higher end-tidal CO₂; this strategy facilitated more stable alveolar recruitment, as evidenced by higher dynamic compliance. Static compliance did not differ significantly between groups, implying that short-term exposure to modest hypercarbia does not adversely affect the elastic recoil of lung parenchyma(Table 5). Hemodynamically, permissive hypercarbia was well tolerated. No significant alterations in mean arterial pressure, heart rate, or CVP were noted. Furthermore, lactate levels and pH remained within physiological ranges, underlining that hypercarbia was not associated with systemic hypoperfusion or severe acidosis during the intraoperative window. Representative Tables Table 1. Demographic Data and Clinical Characteristics (Summary) Variable Normocarbia (n=37) Hypercarbia (n=37) p-value Age (years) 42.08 ± 18.57 39.05 ± 13.32 0.423 Gender (F/M) 12/25 17/20 0.341 Weight (kg) 53.92 ± 6.45 52.59 ± 3.44 0.395 ASA (Grade 1 / Grade 2) 21/15 26/11 0.412 FVC (L) 3.28 ± 0.78 3.25 ± 0.73 0.878 FEV₁ (L) 2.55 ± 0.62 2.58 ± 0.55 0.858 (Table.1) Demographic profile. Table 2. Comparison of Key ABG Parameters During OLV Parameter Normocarbia (n=37) Hypercarbia (n=37) p-value pH 7.35 ± 0.06 6.99 ± 1.37 0.114 PaCO₂ (mmHg) 38.51 ± 2.47 46.86 ± 1.4 <0.001 (S) PaO₂ (mmHg) 295.46 ± 118.41 366.38 ± 117.28 0.012 (S) PaO₂/FiO₂ Ratio 5.91 ± 2.37 7.33 ± 2.35 0.012 (S) (Table.2 ).Hypercarbia group shows a statistically significant increase in Pao2 and Pao2/Fio2 ratio. Table 3. Oxygen Content and Delivery Parameter Normocarbia (n=37) Hypercarbia (n=37) p-value CaO₂ (mL O₂ dL-1) 14.46 ± 1.58 16.16 ± 1.99 <0.001 (S) DO₂ (mL min-1) 62.78 ± 20.1 71.81 ± 17.03 0.41 ) (Table.3) Increased arterial oxygen content (CaO₂) and oxygen delivery (DO₂) in both groups. Table 4: Comparison of respiratory variables among study groups Characteristics Normocarbia Hypercarbia P value Peak inspiratory Pressure (cmH2O) 24.51 ± 4.06 21.86 ± 3.58 0.004 (S) Respiratory rate 15.59 ± 3.03 10.84 ± 2.09 0.001 (S) Tidal volume 281.32 ± 40.56 345 ± 55.36 0.001 (S) (Table.4) Showing decreased Peak inspiratory pressure(PiP) in the hypercarbia group. Table 5: Comparison of dynamic & static compliance (ml/cmH2O) among study groups Characteristics Normocarbia Hypercarbia P value Dynamic compliance 21.59 ± 3.99 25.41 ± 4.49 <0.001 (S) Static compliance 30.86 ± 5.47 32.73 ± 6.97 0.205 (Table 4.) Increased Dynamic and Static compliance in the Hypercarbia group. Acknowledgement: The authors thank the surgical and nursing staff of Cardiothoracic and Vascular Surgery, Sawai Man Singh Medical College, Jaipur. Figure 2. Comparison of mean PaO₂ (mmHg) between Normocarbia and Hypercarbia groups during OLV. Figure 2. shows significantly higher PaO₂ in the hypercarbia group, indicating improved arterial oxygenation during OLV. Permissive hypercarbia may enhance V/Q matching and pulmonary gas exchange efficiency.  Figure 3. Comparison of CaO₂ and DO₂ Between Normocarbia and Hypercarbia A comparative bar chart showing arterial oxygen content (CaO₂) and oxygen delivery (DO₂) between the normocarbia and hypercarbia groups. This visualization directly supports the study’s key finding: permissive hypercarbia enhances oxygen transport capacity during one-lung ventilation.

One-lung ventilation (OLV) is a cornerstone of thoracic anaesthesia, as it provides the surgical team with optimal exposure of the operative lung . However, OLV commonly impairs gas exchange and predisposes patients to arterial hypoxemia and potential hypercarbia . Previous investigations have highlighted the propensity for atelectasis in the dependent lung during OLV, further exacerbating ventilation–perfusion (V/Q) mismatch. In our study, PaO2 was increased during hypercarbia than normocarbia in all patients and pH was reduced during hypercarbia although it was not significant. Dynamic compliance and static compliance were also higher during hypercarbia than normocarbia but dynamic compliance was significantly increased. However, CaO2 and DO2 were substantially higher during hypercarbia than during normocarbia. Peak inspiratory pressure was noticeably reduced during hypercarbia than normocarbia. These results were considered as positive effects on gas exchange during OLV. Arterial oxygenation Arterial oxygen was elevated in Group B as compared to Group A. In a previous study done by Lee et al also observed increase in PaO2 during permissive hypercapnia11. PaO₂/FiO₂ Ratio Was elevated in Group B which was similar to Lee et al indicating improved lung oxygenation with permissive hypercarbia 11. Airway pressures Normocarbia group showed slightly higher peak and mean airway pressures, possibly due to the higher respiratory rates needed to maintain normocarbia. The peak inspiratory pressure decreased in the hypercarbia group as compared to normocarbia. Lee et al also. showed decreased Peak inspiratory pressure which is similar to our study11 . Ventilatory rate significantly decreased in hypercarbia compared to normocarbia and tidal volume was significantly increased during hypercarbia than normocarbia, increased in dynamic compliance, static compliance significantly also showed increased CaO2, increased DO2 which is similar to our study. PH Although the mean pH was lower in Group B, the difference did not reach statistical significance. Kim et al11 observed median pH dropped in moderate hypercapnia. In our study PH decreased from 7.35 to 6.99 which was similar to Lee et al11. which showed increase in PaO2 which is due to hypercarbia causing positive effects in the management of arterial hypoxemia with increased CaO2 and DO2 . Lactate Levels In our study blood lactate concentration was lower during hypercarbia than normocarbia, although the values were considered within normal ranges which was similar to Lee et al 11 study. Dynamic Compliance (Cdyn) Higher in the hypercarbia group. The study found that dynamic lung compliance increased significantly during hypercarbia compared to normocarbia. El-Dawlatly et al12 observed that CO₂ insufflation led to a significant decrease in dynamic lung compliance, highlighting the importance of monitoring and managing ventilatory parameters during such procedures. Static Compliance (C stat) Was higher in Group B in our study. Broccard et al13 demonstrated that hypercapnic acidosis improved static lung compliance and reduced lung injury which suggests that hypercapnic acidosis may have protective effects on lung mechanics during mechanical ventilation. Hemodynamic and Metabolic Parameters Both remained within 20% of baseline values and did not differ significantly between groups which was similar to Kim et al11 study showing no hemodynamic changes. Carvalho et al14 observed in their study that the cardiovascular tolerance to immediate hypercapnia from a Paco2 near 35mmHg to 60-80 mm Hg with high level of PEEP was stable with hemodynamic parameters . Electrolytes No significant differences between groups, remained within clinically acceptable range. Despite the benefits, permissive hypercarbia must be used judiciously. Individuals with intracranial pathology or severe ischemic heart disease may be at risk of worsened intracranial hypertension or hypercapnia-induced arrhythmias14. In the absence of such comorbidities, mild hypercapnia appears to be both safe and effective, as transient respiratory acidosis seldom reaches a level that compromises hemodynamic stability or tissue perfusion15. Additionally, carefully titrated PaCO₂ can actually enhance haemoglobin’s oxygen-release capacity through rightward shifts in the oxyhaemoglobin dissociation curve5. Arterial oxygen content and Oxygen delivery were higher during hypercarbia, suggesting improved pulmonary mechanics and gas exchange. Torbati et al15 also observed that hypercapnia increases blood oxygen-carrying capacity, potentially enhancing systemic oxygen delivery . Michael et al 16 studied the effects of CO2 on rat lung parenchyma and concluded that CO2 caused relaxation of lung parenchyma which led to an improvement in alveolar ventilation to perfusion by increasing the compliance & alveolar ventilation in overperfused (high CO2) regions and decreased alveolar ventilation in under perfused areas which are elevating Pco2 (20-53 mmHg ) produced reversible parenchymal relaxation. CO2 caused a direct effect on tissues which corrected the Va/Q because hypercapnic regions were relaxed and increased Ventilation while hypocapnia regions became stiff and decreased Ventilation . Permissive Hypercarbia is defined as acceptance of increased PCO2 levels and Continuation of ventilation which is usually achieved by either increasing the tidal volume or increasing the RR. Sticher et al17 reported an increase in CI & PVR & decrease in SVR with no change in Oxygenation with hypercarbia hypoventilation during OLV. In this study, they decreased minute ventilation from 8.8 ± 1.7 L min-1 to 4.2 ± 0.70 L min-1 & arterial PaCO2 increased from 41.3 ± 3.0 mmHg to 63.8 ± 7.5 mmHg. During OLV only the dependent, non-collapsed lung is ventilated, and both lungs are perfused. Because the non-ventilated lung is perfused, there is transpulmonary shunting and impairment of oxygenation. This leads to Hypoxaemia and maintaining Sufficient arterial Oxygenation is a challenge for the anesthesiologist. Treatment of Hypoxaemia during OLV is done by either increasing inspiratory Oxygen fraction (fio2), Ventilatory strategy of the lung with or without PEEP, CPAP to the non-ventilated lung by intermittent manual inflation with high-frequency jet ventilation to the non-independent nonventilated lung18 and lastly by pharmacological methods by using regional nebulization with Nitric oxide (NO), Prostaglandin PGE1 (vasodilation of ventilated lung). Studies have shown that infusion of Almitrine alone or associated with nebulization of NO prevents OLV-induced decrease in PaO219,20. Scherer et al21 showed that PAC balloon inflation and PGF-22 infusion were equally effective in improving oxygenation during OLV. Almitrine infusion can be used for Treatment during Hypoxaemia during OLV when standard treatments are ineffective, especially during VATS/thoracoscopic surgeries21. Administrating almitrine 12 microgram kg-1 hr -1for 10 minutes followed by 4 microgram kg -1hr-1 increased arterial oxygenation during OLV in all patients. This is used as an alternative to the ventilation strategy to treat Hypoxaemia during OLV. 22-23 Research showed the effect of Hypercapnic acidosis and hypercapnia with normal PH on HPV showing an increase in HPV during ventilation strategies, whereas Hypercapnic acidosis increased HPV over time. This increased HPV during Hypercapnic acidosis is favourable for lung gas exchange by improving ventilation-perfusion matching and preserving the capillary barrier function.24 Y & Joe et al25 studied patients undergoing elective lung resection surgeries and found that the arterial oxygen partial pressure/ Fractioned oxygen ratio after 60 minutes during OLV Was higher in patients who had a 50 or 60 partial pressure of arterial CO2 group and calculated that permissive hypercarbia increased lung oxygenation during OLV without any postop complication & length of Hospital Stay. Our study is considered as a treatment modality by using permissive hypercarbia as a tool for managing and improving arterial oxygenation during OLV thus treating Hурохаemia during OLV.

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