Alveolar Pressure Research Articles

Physiological Challenges and Adaptations in Competitive Freediving

Competitive freediving is associated with extreme physiologic challenges due to the effects of apnea, submersion in water, and increased ambient pressure. There has nevertheless been a continued progression of world records across freediving disciplines in recent years, with breath-hold times exceeding 10 minutes, and reaching diving depths beyond 200 meters of seawater. The main physiological determinants of breath-hold endurance are the available oxygen stores, i.e., intrapulmonary gas volume, inspired gas concentration, and rate of oxygen consumption. Other factors such as psychological and inherent factors contribute to the individual tolerance to an increasing respiratory stimulus with prolonged breath-hold duration. A freediving athlete must be able to tolerate apnea to stay underwater long enough to reach great distance or depth and resurface safely. Elite freedivers exhibit somewhat remarkable physiological adaptations such as a more pronounced diving-response and hypercapnia tolerance compared to non-divers, as well as metabolic and cerebrovascular adaptations. To reach great depths, elite freedivers employ a breathing technique called glossophyryngeal insufflation (GI) that is enlarging the ratio of total lung capacity to residual volume, thus, mitigating risk of lung squeeze and increasing intrapulmonary gas volume, and thereby enhancing available oxygen stores. Pulmonary anatomy and physiology could not be accounted to restrict the breath-hold diving depths achieved by competitive athletes. However, the acutely increased intrapulmonary pressure during GI is transmitted to the pulmonary vasculature, thereby eliciting a right ventricular pressure overload, and left ventricular dysfunction that may augment hypotension and syncope during glossopharyngeal insufflation. Due to extreme diffusion gradients between alveolar pN2 and N2 pressures in the body tissues at great depth, N2 will be forced into blood and body tissues during descent, elevating risk of N2 narcosis and decompression illness during deep dives. Breath-hold training and preparation have been shown to enhance breath-hold performance. This review highlights recent data on the profound cardiovascular, respiratory, and gas exchange effects that are observed in competitive freedivers, and discusses possible adaptations and risks for humans.

Equine exercise-induced pulmonary hemorrhage: the role of high left-heart pressures secondary to exercise-induced hypervolemia, and high inspiratory pressures.

Exercise-induced hypervolemia is normal in racehorses. Stress failure of the blood-gas barrier causes EIPH and occurs when the transmural pulmonary capillary (Pcap)-alveolar pressure difference (Ptm) exceeds the barrier's stress failure threshold. Why Pcap increases is incompletely understood. We hypothesized that alterations in blood volume (BV) affect left ventricular (LV) and pulmonary arterial wedge (PAW) pressures, and Pcap, and correspondingly affect EIPH severity. Six thoroughbreds with EIPH underwent treadmill exercise at the same speed (≈11.9m/s [11.1, 12.2]; median [IQR]) before (≈119%V̇O2max; B), 2hr after 14L depletion of blood (≈132%V̇O2max; D) and 2hr after reinfusing the blood (≈111%V̇O2max; R). LV, pulmonary arterial (PAP), PAW and intrapleural (Ppl) pressures were measured throughout exercise. Pcap = (PAP+PAW)/2 and Ptm = Pcap - Ppl. EIPH severity was assessed 60min post-exercise by tracheoendoscopy (EIPHgrade) and bronchoalveolar lavage erythrocyte count (BALRBC). A mixed-effect model and Tukey post-hoc test analyzed effects of BV changes on LV, PAW, Pcap, Ppl, Ptm and EIPH. p≤0.05 was significant. EIPH severity was affected by BV (EIPHgrade: p=0.01, BALRBC: p=0.003). Peak Ptm was not different between B (146mmHg [140; 151]) and R (151mmHg [137; 160]) but was lower for D (128mmHg [127; 130]; B: p=0.005, R: p=0.02). LV end diastolic pressure (LVED) was correlated with maxPcap (r2=0.52, p=0.001). Ppl was unaffected by changes in BV. Vascular pressures and Ppl fluctuated constantly during exercise and independently influenced Ptm. Circulating BV but not exercise intensity had a major effect on LVED, Pcap and Ptm, and was correlated with EIPH severity in thoroughbred racehorses (r2=0.48, p=0.001).

Ulcerative colitis complicating pneumomediastinum, subcutaneous emphysema and pneumothorax.

A 17-year-old man with ulcerative colitis (UC) presented to our hospital with neck pain and fever after vomiting. On examination, a snowflake sensation was noted in the neck. A chest radiograph showed extensive subcutaneous emphysema in the chest. CT scans showed extensive subcutaneous emphysema in the neck, shoulders and axilla, as well as pneumomediastinum and pneumothorax. A diagnosis of pneumomediastinum with exacerbation of UC was made, and he was fasted and treated with antibiotics. Intensive granulocyte and monocyte adsorption apheresis (GMA) was started for exacerbation of UC. His symptoms and the radiological findings of pneumomediastinum improved. He remained in remission on azathioprine. UC is a chronic inflammatory bowel disease (IBD) associated with extraintestinal manifestations (EIM). Very few cases have been complicated by pneumomediastinum. The increase in alveolar pressure due to vomiting and systemic inflammation-related pleural or esophageal damage may cause pneumomediastinum in this case. Prevention of progression to mediastinitis and treatment of exacerbated UC are contradictory. GMA was successful because it was not an immunosuppressive therapy. Our case highlights that rare EIM may complicate exacerbation of UC.

Flow interruption compared to forced oscillatory maneuvers and esophageal balloon/pneumotachography for measurement of respiratory resistance in the horse.

Pulmonary function testing is critical to the diagnosis of equine asthma (EA), an important cause of respiratory disease in the horse, but its clinical use has remained elusive, unfortunately, due to the complexity of reference methods, esophageal balloon/pneumotachography (EBP), and forced oscillatory mechanics (FOM), so we sought a noninvasive, portable method for use in horses through rapid interruption of airflow for equilibration of alveolar pressure with proximal airway pressure, termed flow interruption (FI). Resistance (RINT) was computed as the relationship between the change in pressure at the nose before and immediately after interruption and flow immediately before interruption. A pilot study in five healthy university-owned animals using EBP and FI showed good correspondence between the two methods: RINT (0.33 ± 0.05 cmH2O/L/s) and RL (0.31 ± 0.06 cmH2O/L/s). In two separate populations of client-owned horses, with random assignment of methods to FI versus EBP (n = 8), RINT showed good correlation with RL in horses (rs = 0.995, P = 0.0002) and accords with RL, with no significant difference between RINT and RL. Using FOM (n = 12), RINT (0.67 ± 0.31 cmH2O/L/s) has good correlation with RRS measured with FOM (r = 0.834, P = 0.0001), but is consistently smaller than RRS (0.74 ± 0.33 cmH2O/L/s). Histamine bronchoprovocation (HBP) was performed in a subset of these horses: FI classified one horse in six as less reactive than did EBP, and FI classified one horse in seven as less reactive than did FOM.NEW & NOTEWORTHY We developed and document for the first time the use of flow interruption for the rapid and noninvasive measurement of resistance in equine patients and demonstrated short- and long-term stability and accuracy in comparison with the reference methods.

PULMONARY HYPERTENSION DOES NOT LIMIT TRANSLATIONAL APPROACHES OF HYPOXIA MEDIATED MYOCARDIAL REGENERATION

Objective: In mice, prolonged exposure to severe ambient hypoxia promotes myocardial regeneration suggesting a novel treatment target for patients following myocardial infarction. However, hypoxia-induced pulmonary hypertension and myocardial ischemia are potential risks in human studies. Therefore, we conducted a pilot study in carefully selected patients with left ventricular scars to test the cardiovascular safety of prolonged exposure to severe hypoxia. Design and method: At the DLR:envihab facility, we enrolled three male patients with 49-126 months past history of myocardial infarction and one healthy man. Patients had an ejection fraction of 47±7%. We applied incremental ambient hypoxia using nitrogen dilution until alveolar oxygen partial pressure had decreased to 35 mmHg. Then, we maintained atmosphere conditions for 14 days (FiO2=0.095) but added 1% oxygen during the night. We assessed right ventricular function and systolic pulmonary artery pressure at baseline, during hypoxia, and 3 days after recovery in normoxia with transthoracic echocardiography. In venous blood samples, we measured high-sensitivity cardiac troponin T, N-terminal pro-B-type natriuretic peptide (NT-proBNP), and glomerular filtration rate (CystatinC) throughout the study. Results: We observed no clinical signs of heart failure throughout the study. Hypoxia increased systolic pulmonary artery pressure, which rapidly normalized during recovery (baseline: 35±3 mmHg hypoxia: 47±9 recovery: 28±1, p=0.029). Tricuspid annular plane systolic excursion was 28±3 mmHg at baseline, 26±1 mmHg in hypoxia, and 29±2 mmHg during recovery (p=0.069). Right ventricular free wall strain -22.4±3.9 mmHg at baseline, -24±5.4 in hypoxia, and -22.7±1.5 during recovery (p=0.84). Glomerular filtration rate was reduced in hypoxia, but recovered at 30 days follow-up. Troponin remained in the reference range throughout the study and NTproBNP was decreased following hypoxia (p=0.047). Conclusions: In highly selected patients with left ventricular scars, prolonged severe normobaric hypoxia while eliciting pulmonary hypertension did not lead to right heart failure or myocardial damage. Our study provides important information regarding safety of exposing patients to hypoxia in clinical studies or during activities at high altitude.

Mean airway pressure as a parameter of lung-protective and heart-protective ventilation

Mean airway pressure (MAP) is the mean pressure generated in the airway during a single breath (inspiration + expiration), and is displayed on most anaesthesia and intensive care ventilators. This parameter, however, is not usually monitored during mechanical ventilation because it is poorly understood and usually only used in research. One of the main determinants of MAP is PEEP. This is because in respiratory cycles with an I:E ratio of 1:2, expiration is twice as long as inspiration. Although MAP can be used as a surrogate for mean alveolar pressure, these parameters differ considerably in some situations. Recently, MAP has been shown to be a useful prognostic factor for respiratory morbidity and mortality in mechanically ventilated patients of various ages. Low MAP has been associated with a lower incidence of 90-day mortality, shorter ICU stay, and shorter mechanical ventilation time. MAP also affects haemodynamics: there is evidence of a causal relationship between high MAP and low perfusion index, both of which are associated with poor prognosis in mechanically ventilated patients. Elevated MAP values have also been associated with high central venous pressure and lactate, which are indicative of ventilator-associated right ventricular failure and tissue hypoperfusion, respectively. MAP, therefore, is an important parameter to measure in clinical practice. The aim of this review has been to identify the determinants of MAP, the pros and cons of using MAP instead of traditional protective ventilation parameters, and the evidence that supports the use of MAP in clinical practice.

Presión media de la vía aérea: ¿parámetro integrador de ventilación pulmonar y circulatoria protectoras?

Mean airway pressure (MAP) is the mean pressure generated in the airway during a single breath (inspiration+expiration), and is displayed on most anaesthesia and intensive care ventilators. This parameter, however, is not usually monitored during mechanical ventilation because it is poorly understood and usually only used in research. One of the main determinants of MAP is PEEP. This is because in respiratory cycles with an I:E ratio of 1:2, expiration is twice as long as inspiration. Although MAP can be used as a surrogate for mean alveolar pressure, these parameters differ considerably in some situations. Recently, MAP has been shown to be a useful prognostic factor for respiratory morbidity and mortality in mechanically ventilated patients of various ages. Low MAP has been associated with a lower incidence of 90-day mortality, shorter ICU stay, and shorter mechanical ventilation time. MAP also affects haemodynamics: there is evidence of a causal relationship between high MAP and low perfusion index, both of which are associated with poor prognosis in mechanically ventilated patients. Elevated MAP values have also been associated with high central venous pressure and lactate, which are indicative of ventilator-associated right ventricular failure and tissue hypoperfusion, respectively. MAP, therefore, is an important parameter to measure in clinical practice. The aim of this review has been to identify the determinants of MAP, the pros and cons of using MAP instead of traditional protective ventilation parameters, and the evidence that supports the use of MAP in clinical practice.

SMOKING AND FLAP SURVIVAL: A COMPREHENSIVE SYSTEMATIC REVIEW

Background: Free flap reconstruction of complex and/or large wounds, whether traumatic, following cancer resection, or for other reconstructive needs has become a commonly accepted practice. Multiple different types of free flaps are utilized for varying needs based on the individual patient and the defect that requires coverage. active smokers who underwent a nonelective traumatic reconstruction with a perforator-based fasciocutaneous flap (anterolateral thigh [ALT] flap) will have a higher incidence of smoking-related complications compared to the use of a muscle-only flap. The aim: The aim of this study to show about smoking and flap survival. Methods: By the Preferred Reporting Items for Systematic Review and Meta-Analysis (PRISMA) 2020, this study was able to show that it met all of the requirements. This search approach, publications that came out between 2014 and 2024 were taken into account. Several different online reference sources, like Pubmed, SagePub, and Google Scholar were used to do this. It was decided not to take into account review pieces, works that had already been published, or works that were only half done. Result: In the PubMed database, the results of our search get 9 articles, whereas the results of our search on SagePub get 441 articles, on Google Scholar 4830 articles. Records remove before screening are 2771, so we get 2509 articles fos screening. After we screened based on record exclude, we compiled a total of 10 papers. We included five research that met the criteria. Conclusion: Smoking decreases the alveolar oxygen pressure and subcutaneous wound tissue oxygen, and nicotine causes vasoconstriction, smokers are more likely to experience flap loss, hematoma, or fat necrosis than non-smokers. Preoperative and post-operative abstinence period of at least 1 week is necessary for smokers who undergo flap operations.

Abstract 14278: 14 Days of Severe, Sustained Normobaric Hypoxic Enhances Left Ventricular Contractility in Patients After Myocardial Infarction

Studies in mice with experimental myocardial infarction revealed, that sustained severe normobaric hypoxia (FiO2=0.07) reactivates cardiomyocyte proliferation and improves left ventricular ejection fraction. Our study aimed to test safety and feasibility in humans and to assess whether hypoxia improves left ventricular contractility in selected patients with myocardial scars following myocardial infarction.Three males, who suffered myocardial infarction 49-126 months prior to study entry, whose capability for hypoxia acclimatization was validated previously and one healthy male control participated in this proof-of-concept study. After preacclimatization we induced severe hypoxia by adding nitrogen until alveolar oxygen partial pressure reached about 35 mmHg. Hypoxia was maintained for 14 consecutive days (FiO2=0.095) and nights (FiO2=0.105). We assessed ventricular function by echocardiographic-derived global longitudinal strain (LVGLS), serum NTproBNP, high-sensitive Troponin I levels, and marker of myocardial repair. Cardiac 18F-FDG-PET-MRI was done at baseline, end of hypoxia exposure, and at 30 days follow-up. LVGLS increased in prior viable myocardium, but also in areas adjacent to the myocardial scar (baseline: -12.57±2.4 %, end of hypoxia: -14.37±2.62% recovery day 3: -14.33±2.72%, 30 days follow-up: -15.2±3.11%, p=0.0182). NTproBNP tended to decrease (baseline: 189±134 pg/ml, end of hypoxia: 127±28 pg/ml, recovery day 3: 114±18 pg/ml, 30 days follow-up: 108±65 pg/ml). These parameters were not affected in the control. MRI-derived left ventricular enddiastolic volume remained unchanged, but end-systolic left ventricular volume decreased in patients (baseline: 108±49 ml, recovery day 3: 92±50 ml, 30 days follow-up: 101±47 ml, p=0.0068). Troponin I remained in the reference range in all participants. The patient with the most pronounced increase in LVGLS revealed a relevant increase in FDG-uptake at the follow-up, which was also observed in areas adjacent to the myocardial scar.Given the small sample size and the selection of patients, our results have to be interpreted with caution. However, the data indicate potentially beneficial hypoxia-mediated effects in selected patients with ischemic heart disease.

Abstract P129: Cardiovascular Safety Of Severe And Sustained Hypoxia Exposure In Physically Fit Patients Following Myocardial Infarction

In mice, hypoxia exposure corresponding to 8000 m altitude over several weeks induced myocardial proliferation and improved left ventricular ejection fraction following myocardial infarction. To enable translation of these findings from mice to patients with myocardial infarction, we determined whether exposure to severe sustained hypoxia is limited by right ventricular failure secondary to hypoxia-induced pulmonary hypertension. We enrolled three men who suffered myocardial infarctions 49-126 months prior to the study (left ventricular ejection fraction 47±7 %) but were otherwise healthy and one male, healthy control person. We induced hypoxia by adding nitrogen to ambient air until alveolar oxygen partial pressure decreased to 35 mmHg. Normobaric hypoxia was then maintained for 14 consecutive days (FiO2=0.095) corresponding to 6062- 6224 m altitude. We added 1% oxygen over night to ameliorate sleep and prevent acute mountain sickness. We conducted echocardiography at baseline, during hypoxia in hypoxic conditions and 3 days after reconditioning. Measurements included right ventricular to atrial pressure gradient as surrogate for pulmonary artery systolic pressure (PAPsys), tricuspid annulus systolic excursion (TAPSE) and right ventricular (RV) free wall strain. Hypoxia induced pulmonary hypertension, that rapidly abated in recovery (baseline: 35±3 mmHg, hypoxia: 47±9, recovery: 28±1, p=0.0292). TAPSE was not reduced by hypoxic exposure (baseline: 28±3 mmHg, hypoxia: 26±1 recovery: 29±2, p=0.0693) and right ventricular free wall strain was maintained (baseline: -22.4±3.9 mmHg, hypoxia: -24±5.4 recovery: -22.7±1.5, p=0.8493). The healthy control person showed similar responses. No signs or symptoms of right heart failure occurred throughout the study. In highly selected patients with myocardial infarction, substantial normobaric hypoxia induced pulmonary hypertension, however, right ventricular function was well preserved. These observations pave the way for translational studies on hypoxia-induced cardiovascular regeneration and may have implications for patients traveling to high altitude.

A Comparison of Proximal and Tracheal Airway Pressures During Pressure Controlled Ventilation.

Airway pressure is usually measured by sensors placed in the ventilator or on the ventilator side of the endotracheal tube (ETT), at the Y-piece. These remote measurements serve as a surrogate for the tracheal or alveolar pressure. Tracheal pressure can only be predicted correctly by using a model that incorporates the pressure at the remote location, the flow through the ETT, and the resistance of the ETT if the latter is a predictable function of Y-piece flow. However, this is not consistently appropriate, and accuracy of prediction is hampered. This in vitro study systematically examined the ventilator pressure in dependence of compliance of the respiratory system (CRS), inspiratory time, and expiratory time during pressure-controlled ventilation by using a small intratracheal pressure sensor and a mechanical lung simulator. Pressures were measured simultaneously at the ventilator outlet, at the Y-piece, and in the trachea during pressure-controlled ventilation with a peak inspiratory pressure of 20 cm H2O and a PEEP of 5 cm H2O while changing CRS (10, 30, 60, 90, and 100 mL/cm H2O) and varying inspiratory time and expiratory time. Tracheal pressures were always lower (maximum 8 cm H2O during inspiration) or higher (maximum 4 cm H2O during expiration) than the pressures measured proximal to the ETT if zero-flow conditions were not achieved at the end of the breathing cycles. Dependent on CRS and the breathing cycle, tracheal pressures deviated from those measured proximal to the ETT under non-zero-flow conditions. Intratracheal pressure and pressure curve dynamics can differ greatly from the ventilator pressure, depending on the ventilator setting and the CRS. The small pressure sensor may be used as a measurement method of tracheal pressure via integration onto an ETT.

A modal definition of ideal alveolar oxygen.

In the three-compartment model of lung ventilation-perfusion heterogeneity (VA/Q scatter), both Bohr dead space and shunt equations require values for central "ideal" compartment O2 and CO2 partial pressures. However, the ideal alveolar gas equation most accurately calculates mixed (ideal and alveolar dead space) PAO2 . A novel "modal" definition has been validated for ideal alveolar CO2 partial pressure, at the VA/Q ratio in a lung distribution where CO2 elimination is maximal. A multicompartment computer model of physiological, lognormal distributions of VA and Q was used to identify modal "ideal" PAO2 , and find a modification of the alveolar gas equation to estimate it across a wide range of severity of VA/Q heterogeneity and FIO2 . This was then validated in vivo using data from a study of 36 anesthetized, ventilated patients with FIO2 0.35-80. Substitution in the alveolar gas equation of respiratory exchange ratio R with achieved excellent agreement (r2 = 0.999) between the calculated ideal PAO2 and the alveolar-capillary Pc'O2 at the modal VO2 point ("modal" Pc'O2 ), across a range of log standard deviation of VA 0.25-1.75, true shunt 0%-20%, overall VA/Q 0.4-1.6, and FIO2 0.18-1.0, where the modeled PaO2 was over 50 mm Hg. Modal ideal PAO2 can be reliably estimated using routine blood gas measurements.

AIRFLOW ANALYSIS OF HUMAN RESPIRATORY SYSTEM AT DIFFERENT PHYSIOLOGICAL CONDITIONS

In this paper, an attempt has been made to analyze the effect of different physiological conditions i.e., rest, moderate and extremely active on the branch Reynolds number, pressure drop, lost work, alveolar partial O2 pressure, airway resistance and surface tension. From the analysis, it has been observed that local Reynolds number and tracheal pressure drop along with the generations of branch. The alveolar O2 pressure and surface tension decrease with the increased activity level. Work lost due to different major and minor losses in the respiratory tract increases with the increase in activity level. A similar trend was also found for the airway resistance i.e., increases with the increase in activity level. A new parameter, Breathing Work Number (BWN) in respiratory mechanics is introduced. BWN is the ratio of the work of breathing to the sum of work of breathing and work loss, which might find a significant application to denote the respiratory health. From the analysis, it is found that BWN decreases with the increase in activity level.

SAMAY S24: a novel wireless 'online' device for real-time monitoring and analysis of volumetric capnography.

Volumetric capnography (VCap) provides information about CO2 exhaled per breath (VCO2br) and physiologic dead space (VDphys). A novel wireless device with a high response time CO2 mainstream sensor coupled with a digital flowmeter was designed to monitor all VCap parameters online in rabbits (SAMAY S24).Ten New Zealand rabbits were anesthetized and mechanically ventilated. VCO2br corresponds to the area under the VCap curve. We used the modified Langley method to assess the airway VD (VDaw) and the alveolar CO2 pressure. VDphys was estimated using Bohr's formula, and the alveolar VD was calculated by subtracting VDaw from VDphys. We compared (Bland-Altman) the critical VCap parameters obtained by SAMAY S24 (Langley) with the Functional Approximation based on the Levenberg-Marquardt Algorithm (FA-LMA) approach during closed and opened chest conditions.SAMAY S24 could assess dead space volumes and VCap shape in real time with similar accuracy and precision compared to the 'offline' FA-LMA approach. The opened chest condition impaired CO2 kinetics, decreasing the phase II slope, which was correlated with the volume of CO2 exhaled per minute.

Concept of stress and strain in pediatric mechanical ventilation

Studies have shown that the airway pressures displayed on the screen of the ventilator monitor do not correlate with the actual alveolar distending pressures known as transpulmonary pressure or stress. The change in tidal volume (Vt) on top of the available functional residual capacity (FRC), also known as strain, is an essential factor directly related to stress. Even the correlation of driving pressure (DP) with ventilator-induced lung injury (VILI) needs to be interpreted in the background of what Vt, respiratory compliance (Crs) and at what positive end-expiratory pressure (PEEP) is that DP calculated and at what was the chest wall compliance, and the flow rate at that time. Stress and strain are related to all these factors, either directly or indirectly. The impact of stress and strain should be interpreted in “dynamic terms” over time rather than at one point. Hence, VILI is minimized by optimizing the Strain (using appropriate PEEP and Vt against available FRC) and stress (transpulmonary inspiratory and expiratory pressures), applied at an optimal respiratory rate and flow. In the pediatric age group, pulmonary mechanics also change as age changes. Moreover, children respond differently to lung injury than adults, adding another layer of complexity to the concept of stress and strain in the pediatric population. Despite this, most knowledge about stress and strain has come from studies in the adult population. Therefore, more extensive studies focussing on pediatric age groups are needed to improve our understanding of stress and strain in pediatric ventilated patients.

Efficacy of endotracheal tube clamping to prevent positive airways pressure loss and pressure behavior after reconnection: a bench study

BackgroundEndotracheal tube (ETT) clamping before disconnecting the patient from the mechanical ventilator is routinely performed in patients with acute respiratory distress syndrome (ARDS) to minimize alveolar de-recruitment. Clinical data on the effects of ETT clamping are lacking, and bench data are sparse. We aimed to evaluate the effects of three different types of clamps applied to ETTs of different sizes at different clamping moments during the respiratory cycle and in addition to assess pressure behavior following reconnection to the ventilator after a clamping maneuver.MethodsA mechanical ventilator was connected to an ASL 5000 lung simulator using an ARDS simulated condition. Airway pressures and lung volumes were measured at three time points (5 s, 15 s and 30 s) after disconnection from the ventilator with different clamps (Klemmer, Chest-Tube and ECMO) on different ETT sizes (internal diameter of 6, 7 and 8 mm) at different clamping moments (end-expiration, end-inspiration and end-inspiration with tidal volume halved). In addition, we recorded airway pressures after reconnection to the ventilator. Pressures and volumes were compared among different clamps, different ETT-sizes and the different moments of clamp during the respiratory cycle.ResultsThe efficacy of clamping depended on the type of clamp, the duration of clamping, the size of the ETT and the clamping moment. With an ETT ID 6 mm all clamps showed similar pressure and volume results. With an ETT ID 7 and 8 mm only the ECMO clamp was effective in maintaining stable pressure and volume in the respiratory system during disconnection at all observation times. Clamping with Klemmer and Chest-Tube at end inspiration and at end inspiration with halved tidal volume was more efficient than clamping at end expiration (p < 0.03). After reconnection to the mechanical ventilator, end-inspiratory clamping generated higher alveolar pressures as compared with end-inspiratory clamping with halved tidal volume (p < 0.001).ConclusionsECMO was the most effective in preventing significant airway pressure and volume loss independently from tube size and clamp duration. Our findings support the use of ECMO clamp and clamping at end-expiration. ETT clamping at end-inspiration with tidal volume halved could minimize the risk of generating high alveolar pressures following reconnection to the ventilator and loss of airway pressure under PEEP.

Effects of lithotomy and prone positions on hemodynamic parameters, respiratory mechanics, and arterial oxygenation in percutaneous nephrolithotomy performed under general anesthesia.

The position of the body during surgery may affect the patient's body functions, especially the hemodynamic parameters. We aimed to comparatively analyze the effects of lithotomy and prone position on respiratory mechanics, arterial oxygenation, and hemodynamic parameters in patients who underwent percutaneous nephrolithotomy (PNL).

Unlocking the depths: multiple factors contribute to risk for hypoxic blackout during deep freediving

PurposeTo examine the effect of freediving depth on risk for hypoxic blackout by recording arterial oxygen saturation (SpO2) and heart rate (HR) during deep and shallow dives in the sea.MethodsFourteen competitive freedivers conducted open-water training dives wearing a water-/pressure proof pulse oximeter continuously recording HR and SpO2. Dives were divided into deep (> 35 m) and shallow (10–25 m) post-hoc and data from one deep and one shallow dive from 10 divers were compared.ResultsMean ± SD depth was 53 ± 14 m for deep and 17 ± 4 m for shallow dives. Respective dive durations (120 ± 18 s and 116 ± 43 s) did not differ. Deep dives resulted in lower minimum SpO2 (58 ± 17%) compared with shallow dives (74 ± 17%; P = 0.029). Overall diving HR was 7 bpm higher in deep dives (P = 0.002) although minimum HR was similar in both types of dives (39 bpm). Three divers desaturated early at depth, of which two exhibited severe hypoxia (SpO2 ≤ 65%) upon resurfacing. Additionally, four divers developed severe hypoxia after dives.ConclusionsDespite similar dive durations, oxygen desaturation was greater during deep dives, confirming increased risk of hypoxic blackout with increased depth. In addition to the rapid drop in alveolar pressure and oxygen uptake during ascent, several other risk factors associated with deep freediving were identified, including higher swimming effort and oxygen consumption, a compromised diving response, an autonomic conflict possibly causing arrhythmias, and compromised oxygen uptake at depth by lung compression possibly leading to atelectasis or pulmonary edema in some individuals. Individuals with elevated risk could likely be identified using wearable technology.

Improved ventilation efficiency due to continuous gas flow compared to decelerating gas flow in mechanical ventilation: results of a porcine trial.

In pressure-controlled ventilation (PCV), a decelerating gas flow pattern occurs during inspiration and expiration. In contrast, flow-controlled ventilation (FCV) guarantees a continuous gas flow throughout the entire ventilation cycle where the inspiration and expiration phases are simply performed by a change of gas flow direction. The aim of this trial was to highlight the effects of different flow patterns on respiratory variables and gas exchange. Anesthetized pigs were ventilated with either FCV or PCV for 1 h and thereafter for 30 min each in a crossover comparison. Both ventilation modes were set with a peak pressure of 15 cmH2O, positive end-expiratory pressure of 5 cmH2O, a respiratory rate of 20/min, and a fraction of inspired oxygen at 0.3. All respiratory variables were collected every 15 min. Tidal volume and respiratory minute volume were significantly lower in FCV (n = 5) compared with PCV (n = 5) animals [4.6 vs. 6.6, MD -2.0 (95% CI -2.6 to -1.4) mL/kg; P < 0.001 and 7.3 vs. 9.5, MD -2.2 (95% CI -3.3 to -1.0) L/min; P = 0.006]. Notwithstanding these differences, CO2-removal as well as oxygenation was not inferior in FCV compared with PCV. Mechanical ventilation with identical ventilator settings resulted in lower tidal volumes and consecutive minute volume in FCV compared with PCV. This finding can be explained physically by the continuous gas flow pattern in FCV that necessitates a lower alveolar pressure amplitude. Interestingly, gas exchange was comparable in both groups, which is suggestive of improved ventilation efficiency at a continuous gas flow pattern.NEW & NOTEWORTHY This study examined the effects of a continuous (flow-controlled ventilation, FCV) vs. decelerating (pressure-controlled ventilation, PCV) gas flow pattern during mechanical ventilation. It was shown that FCV necessitates a lower alveolar pressure amplitude leading to reduced applied tidal volumes and consequently minute volume. Notwithstanding these differences, CO2-removal as well as oxygenation was not inferior in FCV compared with PCV, which is suggestive of improved gas exchange efficiency at a continuous gas flow pattern.

Flow-controlled expiration reduces positive end-expiratory pressure requirement in dorsally recumbent, anesthetized horses.

Equine peri-anesthetic mortality is higher than that for other commonly anesthetized veterinary species. Unique equine pulmonary pathophysiologic aspects are believed to contribute to this mortality due to impairment of gas exchange and subsequent hypoxemia. No consistently reliable solution for the treatment of peri-anesthetic gas exchange impairment is available. Flow-controlled expiration (FLEX) is a ventilatory mode that linearizes gas flow throughout the expiratory phase, reducing the rate of lung emptying and alveolar collapse. FLEX has been shown to improve gas exchange and pulmonary mechanics in anesthetized horses. This study further evaluated FLEX ventilation in anesthetized horses positioned in dorsal recumbency, hypothesizing that after alveolar recruitment, horses ventilated using FLEX would require a lower positive end-expiratory pressure (PEEP) to prevent alveolar closure than horses conventionally ventilated. Twelve adult horses were used in this prospective, randomized study. Horses were assigned either to conventional volume-controlled ventilation (VCV) or to FLEX. Following induction of general anesthesia, horses were placed in dorsal recumbency mechanically ventilated for a total of approximately 6.5 hours. Thirty-minutes after starting ventilation with VCV or FLEX, a PEEP-titration alveolar recruitment maneuver was performed at the end of which the PEEP was reduced in decrements of 3 cmH2O until the alveolar closure pressure was determined. The PEEP was then increased to the previous level and maintained for additional three hours. During this time, the mean arterial blood pressure, pulmonary arterial pressure, central venous blood pressure, cardiac output (CO), dynamic respiratory system compliance and arterial blood gas values were measured. The alveolar closure pressure was significantly lower (6.5 ± 1.2 vs 11.0 ± 1.5 cmH2O) and significantly less PEEP was required to prevent alveolar closure (9.5 ± 1.2 vs 14.0 ± 1.5 cmH2O) for horses ventilated using FLEX compared with VCV. The CO was significantly higher in the horses ventilated with FLEX (37.5 ± 4 vs 30 ± 6 l/min). We concluded that FLEX ventilation was associated with a lower PEEP requirement due to a more homogenous distribution of ventilation in the lungs during expiration. This lower PEEP requirement led to more stable and improved cardiovascular conditions in horses ventilated with FLEX.