The Effect of Volume Controlled and Pressure Controlled Ventilation Modes on Cerebral Oximetry and Blood Gas Status in Laparoscopic Cholecystectomy, A Randomized Controlled Trial

Background: To compare the volume-controlled and pressure-controlled ventilation modes with near infrared spectroscopy (NIRS) cerebral oximetry and blood gas status in laparoscopic cholecystectomyMethods: Seventy patients (n=70), who underwent elective laparoscopic cholecystectomy operation were randomized into two groups (volume control ventilation - group V, pressure control ventilation - group P). Demographic data (age, gender, body mass index) and operative data (anesthesia, surgery, and insufflation durations) were recorded. Patients’ single derivation electrocardiogram, pulse oximetry, non-invasive arterial pressure, NIRS cerebral oximetry and end-tidal CO2 parameters were recorded. Measurements were done at the start of anesthesia (T0), at the end of intubation (T1), 5 minutes after the insufflation (T2), at the time just before desufflation (T3) and 5 minutes after desufflation (T4).The patients’ heart rate, systolic and diastolic arterial pressure, saturation of pulse oximetry, and NIRS values were recorded for time points. Additionally, arterial gas results and mechanical ventilation parameters were recorded as well. Results: No significant difference was found in age, sex, body mass index. Operation, anesthesia and insufflation durations were similar for the groups. In Group P, NIRS right T1-2-3 averages and NIRS left T2-3 averages were significantly higher than Group V (p=0.030, p=0.001, p=0.001, p=0.006, p=0.002 respectively). In Group P T1-T2-T4, mean peak pressures and mean plateau pressures were significantly lower than Group V (p=0.003, p=0.001, p<0.001, p=0.011, p=0.001, p<0.001 respectively).Conclusion: Mechanical ventilation that performed in pressure-control ventilation mode is resulted with better tissue oxygenation than volume-control ventilation mode. In pressure-control ventilation mode, peak pressure and plateau pressure were lower.Registration of study at ClinicalTrials.gov was made at 25/01/2021 with the NCT04723043 number.

Changes in dead space components during pressure-controlled inverse ratio ventilation: A secondary analysis of a randomized trial

Background We previously reported that there were no differences between the lung-protective actions of pressure-controlled inverse ratio ventilation and volume control ventilation based on the changes in serum cytokine levels. Dead space represents a ventilation-perfusion mismatch, and can enable us to understand the heterogeneity and elapsed time changes in ventilation-perfusion mismatch. Methods This study was a secondary analysis of a randomized controlled trial of patients who underwent robot-assisted laparoscopic radical prostatectomy. The inspiratory to expiratory ratio was adjusted individually by observing the expiratory flow-time wave in the pressure-controlled inverse ratio ventilation group (n = 14) and was set to 1:2 in the volume-control ventilation group (n = 13). Using volumetric capnography, the physiological dead space was divided into three dead space components: airway, alveolar, and shunt dead space. The influence of pressure-controlled inverse ratio ventilation and time factor on the changes in each dead space component rate was analyzed using the Mann-Whitney U test and Wilcoxon’s signed rank test. Results The physiological dead space and shunt dead space rate were decreased in the pressure-controlled inverse ratio ventilation group compared with those in the volume control ventilation group (p < 0.001 and p = 0.003, respectively), and both dead space rates increased with time in both groups. The airway dead space rate increased with time, but the difference between the groups was not significant. There were no significant changes in the alveolar dead space rate. Conclusions Pressure-controlled inverse ratio ventilation reduced the physiological dead space rate, suggesting an improvement in the total ventilation/perfusion mismatch due to improved inflation of the alveoli affected by heterogeneous expansion disorder without hyperinflation of the normal alveoli. However, the shunt dead space rate increased with time, suggesting that atelectasis developed with time in both groups.

Diaphragm neurostimulation during mechanical ventilation reduces atelectasis and transpulmonary plateau pressure, preserving lung homogeneity and PaO2/FiO2

Tidal volume delivered by mechanical ventilation to a sedated patient is distributed in a non-physiological pattern, causing atelectasis (underinflation) and overdistension (overinflation). Activation of the diaphragm during mechanical ventilation provides a way to reduce atelectasis and alveolar inhomogeneity, protecting the lungs from ventilator-induced lung injury while also protecting the diaphragm by preventing ventilator-induced diaphragm dysfunction. We studied the hypothesis that diaphragm contractions elicited by transvenous phrenic nerve stimulation, delivered in synchrony with volume-control ventilation, would reduce atelectasis and lung inhomogeneity in a healthy, normal-lung pig model. Twenty-five large pigs were ventilated for 50 hours with lung-protective volume-control ventilation combined with synchronous transvenous phrenic-nerve neurostimulation on every breath, or every second breath. This was compared to lung-protective ventilation alone. Lung mechanics and ventilation pressures were measured using esophageal pressure manometry and electrical impedance tomography. Alveolar homogeneity was measured using alveolar chord length of preserved lung tissue. Lung injury was measured using inflammatory cytokine concentration in bronchoalveolar lavage fluid and serum. We found that diaphragm neurostimulation on every breath preserved PaO2/FiO2 and significantly reduced the loss of end-expiratory lung volume after 50 hours of mechanical ventilation. Neurostimulation on every breath reduced plateau and driving pressures, improved both static and dynamic compliance and resulted in less alveolar inhomogeneity. These findings support that temporary transvenous diaphragm neurostimulation during volume-controlled, lung-protective ventilation may offer a potential method to provide both lung- and diaphragm-protective ventilation.

Atelectasis, Shunt, and Worsening Oxygenation Following Reduction of Respiratory Rate in Healthy Pigs Undergoing ECMO: An Experimental Lung Imaging Study

Rationale: Reducing the respiratory rate during extracorporeal membrane oxygenation (ECMO) decreases the mechanical power, but it might induce alveolar de-recruitment. Dissecting de-recruitment due to lung edema vs. the fraction due to hypoventilation may be challenging in injured lungs.Objectives: We characterized changes in lung physiology (primary endpoint: development of atelectasis) associated with progressive reduction of the respiratory rate in healthy animals on ECMO.Methods: Six female pigs underwent general anesthesia and volume control ventilation (Baseline: PEEP 5 cmH2O, Vt 10 ml/kg, I:E = 1:2, FiO2 0.5, rate 24 bpm). Veno-venous ECMO was started and respiratory rate was progressively reduced to 18, 12, and 6 breaths per minute (6-h steps), while all other settings remained unchanged. ECMO blood flow was kept constant while gas flow was increased to maintain stable PaCO2.Measurements and Main Results: At Baseline (without ECMO) and toward the end of each step, data from quantitative CT scan, electrical impedance tomography, and gas exchange were collected. Increasing ECMO gas flow while lowering the respiratory rate was associated with an increase in the fraction of non-aerated tissue (i.e., atelectasis) and with a decrease of tidal ventilation reaching the gravitationally dependent lung regions (p = 0.009 and p = 0.018). Intrapulmonary shunt increased (p &lt; 0.001) and arterial PaO2 decreased (p &lt; 0.001) at lower rates. The fraction of non-aerated lung was correlated with longer expiratory time spent at zero flow (r = 0.555, p = 0.011).Conclusions: Progressive decrease of respiratory rate coupled with increasing CO2 removal in mechanically ventilated healthy pigs is associated with development of lung atelectasis, higher shunt, and poorer oxygenation.