Changes In Transpulmonary Pressure Research Articles

A novel method to quantify breathing effort from respiratory mechanics and esophageal pressure.

Breathing effort is important to quantify to understand mechanisms underlying central and obstructive sleep apnea, respiratory-related arousals, and the timing and effectiveness of invasive or non-invasive mechanically assisted ventilation. Current quantitative methods to evaluate breathing effort rely on inspiratory esophageal or epiglottic pressure swings or changes in diaphragm electromyographic (EMG) activity, where units are problematic to interpret and compare between individuals and to measured ventilation. This paper derives a novel method to quantify breathing effort in units directly comparable to measured ventilation by applying respiratory mechanics first principles to convert continuous transpulmonary pressure measurements into "attempted" airflow expected to have arisen without upper airway obstruction. The method was evaluated using data from eleven subjects undergoing overnight polysomnography, including 6 obese patients with severe obstructive sleep apnea (OSA), including one who also had frequent central events, and 5 healthy-weight controls. Classic respiratory mechanics showed excellent fits of airflow and volume to transpulmonary pressures during wake periods of stable unobstructed breathing (mean ± SD r² = 0.94 ± 0.03), with significantly higher respiratory system resistance in patients compared to healthy controls (11.2 ± 3.3 vs 7.1 ± 1.9 cmH2O·l-1·sec, P=0.032). Subsequent estimates of attempted airflow from transpulmonary pressure changes clearly highlighted periods of acute and prolonged upper airway obstruction, including within the first few breaths following sleep onset in patients. This novel technique provides unique quantitative insights into the complex and dynamically changing inter-relationships between breathing effort and achieved airflow during periods of obstructed breathing in sleep.

PPV May Be a Starting Point to Achieve Circulatory Protective Mechanical Ventilation.

Pulse pressure variation (PPV) is a mandatory index for hemodynamic monitoring during mechanical ventilation. The changes in pleural pressure (Ppl) and transpulmonary pressure (PL) caused by mechanical ventilation are the basis for PPV and lead to the effect of blood flow. If the state of hypovolemia exists, the effect of the increased Ppl during mechanical ventilation on the right ventricular preload will mainly affect the cardiac output, resulting in a positive PPV. However, PL is more influenced by the change in alveolar pressure, which produces an increase in right heart overload, resulting in high PPV. In particular, if spontaneous breathing is strong, the transvascular pressure will be extremely high, which may lead to the promotion of alveolar flooding and increased RV flow. Asynchronous breathing and mediastinal swing may damage the pulmonary circulation and right heart function. Therefore, according to the principle of PPV, a high PPV can be incorporated into the whole respiratory treatment process to monitor the mechanical ventilation cycle damage/protection regardless of the controlled ventilation or spontaneous breathing. Through the monitoring of PPV, the circulation-protective ventilation can be guided at bedside in real time by PPV.

Abstract 9701: Hemodynamic Parameters Deteriorate Over Time, and Relate to Adverse Clinical Outcomes, in Children and Adults with Fontan Circulation

Introduction: In patients with univentricular heart disease, Fontan palliation allows for improved survival. However, Fontan circulatory function deteriorates over time, marked by the onset of functional limitations, morbidities, and mortality. Invasive surveillance offers insights into hemodynamic conditions and may facilitate identification of at-risk patients. Objective: To characterize longitudinal changes in invasive Fontan hemodynamics and evaluate for associations with adverse clinical outcomes. Methods: Single-center retrospective study of serial invasive hemodynamics (≥2 catheterizations) in Fontan patients from 2006-2020. The first and last procedures per patient were analyzed for Fontan pressure, ventricular end diastolic pressure (EDP), cardiac output (CO), systemic (SVR), pulmonary (PVR) and total vascular resistance (TVR). The composite clinical endpoint included death, heart transplant or listing, Fontan takedown, protein losing enteropathy, plastic bronchitis, admission for arrhythmia or congestive heart failure and Fontan revision. Results: Serial hemodynamic evaluations were analyzed in 71 Fontan patients, with first catheterization occurring at median age of 7.1 years (IQR 4.1, 14) and 8.4 years (4.7, 12.3) between assessments. The most common diagnosis was hypoplastic left heart syndrome (45%). Fontan pressure, CO and PVR did not significantly change between assessments, whereas EDP increased by 1.9±3.6 mmHg ( p <0.001). The annualized rate of change in EDP was 0.2±0.14 mmHg/year. SVR (2.0±7.5 U x m 2 , p =0.012) and TVR (2.16 ±7.8 U x m 2 , p =0.031) also increased significantly between assessments. The clinical endpoint was met in 43 (61%) patients and was associated with a greater change in transpulmonary gradient (0.13±1.9 vs -0.87±2.0 mmHg, p =0.046) and Fontan pressure (1.1±5.4 vs -0.7±2.7 mmHg, p =0.066) but not EDP, CO, SVR, PVR or TVR. Conclusion: Over a relatively brief time period, this single-center cohort of Fontan patients demonstrated clinically significant longitudinal increases in EDP, SVR and TVR. Adverse clinical outcomes were common and associated with greater hemodynamic deterioration between assessments. Serial interrogation of Fontan hemodynamics is likely to prove clinically useful.

Early Inspiratory Effort Assessment by Esophageal Manometry Predicts Noninvasive Ventilation Outcome in De Novo Respiratory Failure. A Pilot Study.

Rationale: The role of inspiratory effort still has to be determined as a potential predictor of noninvasive mechanical ventilation (NIV) failure in acute hypoxic de novo respiratory failure.Objectives: To explore the hypothesis that inspiratory effort might be a major determinant of NIV failure in these patients.Methods: Thirty consecutive patients with acute hypoxic de novo respiratory failure admitted to a single center and candidates for a 24-hour NIV trial were enrolled. Clinical features, tidal change in esophageal pressure (ΔPes), tidal change in dynamic transpulmonary pressure (ΔPl), expiratory Vt, and respiratory rate were recorded on admission and 2–4 to 12–24 hours after NIV start and were tested for correlation with outcomes.Measurements and Main Results: ΔPes and ΔPes/ΔPl ratio were significantly lower 2 hours after NIV start in patients who successfully completed the NIV trial (n = 18) compared with those who needed endotracheal intubation (n = 12) (median [interquartile range], 11 [8–15] cm H2O vs. 31.5 [30–36] cm H2O; P < 0.0001), whereas other variables differed later. ΔPes was not related to other predictors of NIV failure at baseline. NIV-induced reduction in ΔPes of 10 cm H2O or more after 2 hours of treatment was strongly associated with avoidance of intubation and represented the most accurate predictor of treatment success (odds ratio, 15; 95% confidence interval, 2.8–110; P = 0.001 and area under the curve, 0.97; 95% confidence interval, 0.91–1; P < 0.0001).Conclusions: The magnitude of inspiratory effort relief as assessed by ΔPes variation within the first 2 hours of NIV was an early and accurate predictor of NIV outcome at 24 hours.Clinical trial registered with www.clinicaltrials.gov (NCT 03826797).

Hemodynamic Effects of Changes in Transpulmonary Pressure During Recruitment Maneuver in Patients Under Pressure Supported Mechanical Ventilation

Hemodynamic Effects of Changes in Transpulmonary Pressure During Recruitment Maneuver in Patients Under Pressure Supported Mechanical Ventilation

Isolated airways in equine respiratory pharmacology: They never lie

Pre-clinical studies on human isolated bronchi have relevant translational value in human in vivo, conversely no investigation has been performed to assess whether data resulting from equine isolated airways can have any translational application in asthmatic horses. Thus, a meta-regression analysis via random-effect method was carried out to correlate the pharmacological characteristics of bronchodilators resulting from experiments performed in equine isolated bronchi with their impact on the lung function outcomes in asthmatic horses. Data on the potency of different bronchodilators were extracted from four ex vivo studies involving 68 horses, and related with the maximum change in transpulmonary pressure (ΔPplmax), pulmonary resistance (RL), and dynamic lung compliance (Cdyn) resulting from the meta-analysis of clinical trials aimed to assess the effect of different bronchodilator classes, namely antimuscarinic agents and β2-adrenoreceptor (β2-AR) agonists, on lung function of asthmatic horses. The potency (pEC50) detected in equine isolated bronchi for each specific bronchodilator did not significantly (P > 0.05) influence the bronchorelaxant effect resulting from clinical trials. RL was characterized by a flatter meta-regression line (slope 0.01, 95%CI -0.25 – 0.28) with respect to ΔPplmax (slope 0.90, 95%CI -4.06 – 2.26) and Cdyn (slope 0.09, 95%CI -0.21 – 0.04). The quality of evidence was moderate for RL and ΔPplmax and low for Cdyn. This quantitative synthesis provides the indirect evidence that pre-clinical investigations performed by using equine isolated airways may produce useful data to predict the impact of bronchodilators on the RL of asthmatic horses. Further translational studies are needed to directly confirm the results of this research.

A novel method for transpulmonary pressure estimation using fluctuation of central venous pressure.

The objective of the study is to develop a correction method for estimating the change in pleural pressure (ΔPpl) and plateau transpulmonary pressure (PL) by using the change in central venous pressure (ΔCVP). Seven children (aged < 15years) with acute respiratory failure (PaO2/FIO2 < 300mmHg), who were paralyzed and mechanically ventilated with a PEEP of < 10 cmH2O and had central venous catheters and esophageal balloon catheters placed for clinical purposes, were enrolled prospectively. We compared change in esophageal pressure (ΔPes), ΔCVP, and ΔPpl calculated using a corrected ΔCVP (cΔCVP-derived ΔPpl). cΔCVP-derived ΔPpl was calculated as κ × ΔCVP, where κ was the ratio of the change in airway pressure (ΔPaw) to ΔCVP during the occlusion test. cΔCVP-derived ΔPpl correlated better than ΔCVP with ΔPes (R2 = 0.48, p = 0.08 vs. R2 = 0.14, p = 0.4) with lesser bias and precision in Bland-Altman analysis. The plateau PL calculated using the cΔCVP-derived ΔPpl (17.6 ± 2.6 cmH2O) correlated well with the ΔPes-derived plateau PL (18.1 ± 2.3 cmH2O) (R2 = 0.90, p = 0.001). Our correction method can estimate ΔPpl and plateau PL from ΔCVP with a reasonable accuracy in paralyzed and mechanically ventilated pediatric patients with respiratory failure.

Clinical efficacy of bronchodilators in equine asthma: Looking for minimal important difference.

Airway obstruction is the main trait of severe equine asthma that affects respiratory function and elicits detrimental effects on clinical presentation. Only few and underpowered clinical studies have investigated the impact of improvement in lung function induced by bronchodilators on the clinical signs of asthma-affected horses. To identify the minimal important difference (MID) in lung function elicited by bronchodilator leading to a meaningful improvement in clinical signs. Pairwise meta-analysis and meta-regression analysis. Literature searches were performed for studies that investigated the effect of bronchodilator therapy on lung function and clinical condition of asthmatic horses. The relationship between the change in lung function variables and clinical score was analysed via random-effect meta-regression. One-point change of the Improved clinically Detectable Equine Asthma Scoring System (IDEASS) score was used to identify the MID. A significant (P<0.05) relationship was found between the changes in IDEASS score and maximum change in transpulmonary pressure (ΔPplmax ) or pulmonary resistance (RL ). Since only the model resulting for RL passed through the origin (Y-intercept when X=0: -0.31, 95% CI -0.75 to 0.14), this variable was used to identify the MID correlated with a meaningful improvement in clinical signs. The resulting MID value was a change in RL of 0.63cmH2 O/L/s (95% CI 0.33-0.94), representing the slope of meta-regression model (high quality of evidence). No long-term studies investigated the effect of bronchodilator agents on both lung function and clinical signs in asthmatic horses. In conclusion, bronchodilator pharmacotherapy in equine asthma elicits clinically meaningful effect when RL increases ≥1cmH2 O/L/s, a value indicating the MID. Assessing the MID based on change in RL may improve the quality of evidence and the scientific impact of future clinical trials as it extends beyond the simple, and limiting, evaluation of statistical significance.

Heart-Lung interaction in spontaneous breathing subjects: the basics

Heart-lung interactions occur primarily because of two components of lung inflation, changes in pleural pressure and changes in transpulmonary pressure. Of these, changes in pleural pressure dominate during spontaneous breathing. Because the heart is surrounded by pleural pressure, during inspiration the environment of the heart falls relative to the rest of the body. This alters inflow into the right heart and outflow from the left heart. Alterations in transpulmonary pressure can alter the outflow from the right heart and the inflow to the left heart. These interactions are modified by the cardiac and respiratory frequency, ventricular function and magnitude of the respiratory efforts.

Physiology-guided management of hemodynamics in acute respiratory distress syndrome.

Skillfully implemented mechanical ventilation (MV) may prove of immense benefit in restoring physiologic homeostasis. However, since hemodynamic instability is a primary factor influencing mortality in acute respiratory distress syndrome (ARDS), clinicians should be vigilant regarding the potentially deleterious effects of MV on right ventricular (RV) function and pulmonary vascular mechanics (PVM). During both spontaneous and positive pressure MV (PPMV), tidal changes in pleural pressure (PPL), transpulmonary pressure (PTP, the difference between alveolar pressure and PPL), and lung volume influence key components of hemodynamics: preload, afterload, heart rate, and myocardial contractility. Acute cor pulmonale (ACP), which occurs in 20-25% of ARDS cases, emerges from negative effects of lung pathology and inappropriate changes in PPL and PTP on the pulmonary microcirculation during PPMV. Functional, minimally invasive hemodynamic monitoring for tracking cardiac performance and output adequacy is integral to effective care. In this review we describe a physiology-based approach to the management of hemodynamics in the setting of ARDS: avoiding excessive cardiac demand, regulating fluid balance, optimizing heart rate, and keeping focus on the pulmonary circuit as cornerstones of effective hemodynamic management for patients in all forms of respiratory failure.

Volume-controlled Ventilation Does Not Prevent Injurious Inflation during Spontaneous Effort

Spontaneous breathing during mechanical ventilation increases transpulmonary pressure and Vt, and worsens lung injury. Intuitively, controlling Vt and transpulmonary pressure might limit injury caused by added spontaneous effort. To test the hypothesis that, during spontaneous effort in injured lungs, limitation of Vt and transpulmonary pressure by volume-controlled ventilation results in less injurious patterns of inflation. Dynamic computed tomography was used to determine patterns of regional inflation in rabbits with injured lungs during volume-controlled or pressure-controlled ventilation. Transpulmonary pressure was estimated by using esophageal balloon manometry [Pl(es)] with and without spontaneous effort. Local dependent lung stress was estimated as the swing (inspiratory change) in transpulmonary pressure measured by intrapleural manometry in dependent lung and was compared with the swing in Pl(es). Electrical impedance tomography was performed to evaluate the inflation pattern in a larger animal (pig) and in a patient with acute respiratory distress syndrome. Spontaneous breathing in injured lungs increased Pl(es) during pressure-controlled (but not volume-controlled) ventilation, but the pattern of dependent lung inflation was the same in both modes. In volume-controlled ventilation, spontaneous effort caused greater inflation and tidal recruitment of dorsal regions (greater than twofold) compared with during muscle paralysis, despite the same Vt and Pl(es). This was caused by higher local dependent lung stress (measured by intrapleural manometry). In injured lungs, esophageal manometry underestimated local dependent pleural pressure changes during spontaneous effort. Limitation of Vt and Pl(es) by volume-controlled ventilation could not eliminate harm caused by spontaneous breathing unless the level of spontaneous effort was lowered and local dependent lung stress was reduced.

Evaluation of oxygen administration with a high-flow nasal cannula to clinically normal dogs.

OBJECTIVE To evaluate the safety and efficacy of oxygen administration by use of a high-flow nasal cannula (HFNC) in sedated clinically normal dogs. ANIMALS 6 healthy adult dogs undergoing routine dental prophylaxis. PROCEDURES Dogs were sedated with butorphanol tartrate and dexmedetomidine. An esophageal balloon catheter was inserted into the esophagus, a double-pronged nasal cannula was inserted into the nares, and a catheter was inserted into the dorsal pedal artery. Dogs were positioned in right lateral recumbency. After a 6-minute acclimation period, baseline blood gas values and transpulmonary pressure were measured. Dogs then received supplemental oxygen via conventional oxygen therapy (COT) at a rate of 100 mL/kg/min (COT-100 treatment) and an HFNC at a rate of 20 L/min (HF-20 treatment) and 30 L/min (HF-30 treatment). Arterial blood gas and transpulmonary pressure were measured after a 6-minute acclimation period for each oxygen delivery method. Radiographs were obtained before and after oxygen administration to evaluate gastric distension. RESULTS Median Pao2 was significantly higher for HF-20 (519.9 mm Hg) and HF-30 (538.1 mm Hg) treatments, compared with median Pao2 for the COT-100 treatment (202.9 mm Hg). The Pao2 did not differ significantly between the HF-20 and HF-30 treatments. There was no significant difference in Paco2 or change in transpulmonary pressure between baseline and any oxygen delivery method. CONCLUSIONS AND CLINICAL RELEVANCE In this study, HFNC appeared to be a safe and effective method for oxygen delivery to sedated healthy dogs. Further studies are needed to evaluate use of HFNCs for oxygen administration to hypoxemic patients.

Pharmacological treatments in asthma-affected horses: A pair-wise and network meta-analysis.

Equine asthma is a disease characterised by reversible airflow obstruction, bronchial hyper-responsiveness and airway inflammation following exposure of susceptible horses to specific airborne agents. Although clinical remission can be achieved in a low-airborne dust environment, repeated exacerbations may lead to irreversible airway remodelling. The available data on the pharmacotherapy of equine asthma result from several small studies, and no head-to-head clinical trials have been conducted among the available medications. To assess the impact of the pharmacological interventions in equine asthma and compare the effect of different classes of drugs on lung function. Pair-wise and network meta-analysis. Literature searches for clinical trials on the pharmacotherapy of equine asthma were performed. The risk of publication bias was assessed by funnel plots and Egger's test. Changes in maximum transpulmonary or pleural pressure, pulmonary resistance and dynamic lung compliance vs. control were analysed via random-effects models and Bayesian networks. The results obtained from 319 equine asthma-affected horses were extracted from 32 studies. Bronchodilators, corticosteroids and chromones improved maximum transpulmonary or pleural pressure (range: -8.0 to -21.4 cmH2 O; P<0.001). Bronchodilators, corticosteroids and furosemide reduced pulmonary resistance (range: -1.2 to -1.9 cmH2 O/L/s; P<0.001), and weakly increased dynamic lung compliance. Inhaled β2 -adrenoreceptor (β2 -AR) agonists and inhaled corticosteroids had the highest probability of being the best therapies. Long-term treatments were more effective than short-term treatments. Weak publication bias was detected. This study demonstrates that long-term treatments with inhaled corticosteroids and long-acting β2 -AR agonists may represent the first choice for treating equine asthma. Further high quality clinical trials are needed to clarify whether inhaled bronchodilators should be preferred to inhaled corticosteroids or vice versa, and to investigate the potential superiority of combination therapy in equine asthma.

Efficacy of Inhaled Levalbuterol Compared to Albuterol in Horses with Recurrent Airway Obstruction.

BackgroundThe (R)‐enantiomer of racemic albuterol (levalbuterol) has bronchodilatory properties whereas the (S)‐enantiomer causes adverse effects in human airways, animal models, and isolated equine bronchi. Levalbuterol is commercially available and improves pulmonary function of asthmatic patients with a longer duration of effect than albuterol.ObjectiveTo determine the dose at which inhaled levalbuterol produces maximal bronchodilatory effect (EDmax) and determine its duration of action in recurrent airway obstruction (RAO)‐affected horses in comparison to racemic albuterol.AnimalsNine horses with inducible and reversible RAO.MethodsRandomized, crossover trial. Horses were challenged with moldy hay to induce airway obstruction. Horses were treated with nebulized albuterol or levalbuterol chosen randomly. Pulmonary function testing (PFT) was measured before and for up to 3 hours after bronchodilatation challenge. Maximum change in transpulmonary pressure (DP max) was measured to assess the dose effect and duration of action of each drug. After a 24 hours washout period, the bronchodilatation challenge was repeated with the second bronchodilator.ResultsThe duration of effect was 60 minutes for albuterol and 120 minutes for levalbuterol. The dose of bronchodilator EDmax was not significantly different between albuterol and levalbuterol (EDmax = 125.0 [125–125 μg] and EDmax = 188 [125–188 μg] respectively; P = .068). The magnitude of bronchodilatation was not significantly different between the 2 treatments (61.1 and 59.9% decrease in DP max for albuterol and levalbuterol respectively; P = .86).Conclusions and clinical importanceLevalbuterol is as effective a bronchodilator as albuterol; although levalbuterol lasts twice as long as albuterol, its duration of action is still too short to make it practical for RAO treatment.

Do spontaneous and mechanical breathing have similar effects on average transpulmonary and alveolar pressure? A clinical crossover study.

BackgroundPreservation of spontaneous breathing (SB) is sometimes debated because it has potentially both negative and positive effects on lung injury in comparison with fully controlled mechanical ventilation (CMV). We wanted (1) to verify in mechanically ventilated patients if the change in transpulmonary pressure was similar between pressure support ventilation (PSV) and CMV for a similar tidal volume, (2) to estimate the influence of SB on alveolar pressure (Palv), and (3) to determine whether a reliable plateau pressure could be measured during pressure support ventilation (PSV).MethodsWe studied ten patients equipped with esophageal catheters undergoing three levels of PSV followed by a phase of CMV. For each condition, we calculated the maximal and mean transpulmonary (ΔPL) swings and Palv.ResultsOverall, ΔPL was similar between CMV and PSV, but only loosely correlated. The differences in ΔPL between CMV and PSV were explained largely by different inspiratory flows, indicating that the resistive pressure drop caused this difference. By contrast, the Palv profile was very different between CMV and SB; SB led to progressively more negative Palv during inspiration, and Palv became lower than the set positive end-expiratory pressure in nine of ten patients at low PSV. Finally, inspiratory occlusion holds performed during PSV led to plateau and Δ PL pressures comparable with those measured during CMV.ConclusionsUnder similar conditions of flow and volume, transpulmonary pressure change is similar between CMV and PSV. SB during mechanical ventilation can cause remarkably negative swings in Palv, a mechanism by which SB might potentially induce lung injury.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-016-1290-9) contains supplementary material, which is available to authorized users.

Experts' opinion on management of hemodynamics in ARDS patients: focus on the effects of mechanical ventilation.

Acute respiratory distress syndrome (ARDS) is frequently associated with hemodynamic instability which appears as the main factor associated with mortality. Shock is driven by pulmonary hypertension, deleterious effects of mechanical ventilation (MV) on right ventricular (RV) function, and associated-sepsis. Hemodynamic effects of ventilation are due to changes in pleural pressure (Ppl) and changes in transpulmonary pressure (TP). TP affects RV afterload, whereas changes in Ppl affect venous return. Tidal forces and positive end-expiratory pressure (PEEP) increase pulmonary vascular resistance (PVR) in direct proportion to their effects on mean airway pressure (mPaw). The acutely injured lung has a reduced capacity to accommodate flowing blood and increases of blood flow accentuate fluid filtration. The dynamics of vascular pressure may contribute to ventilator-induced injury (VILI). In order to optimize perfusion, improve gas exchange, and minimize VILI risk, monitoring hemodynamics is important. During passive ventilation pulse pressure variations are a predictor of fluid responsiveness when conditions to ensure its validity are observed, but may also reflect afterload effects of MV. Central venous pressure can be helpful to monitor the response of RV function to treatment. Echocardiography is suitable to visualize the RV and to detect acute cor pulmonale (ACP), which occurs in 20-25% of cases. Inserting a pulmonary artery catheter may be useful to measure/calculate pulmonary artery pressure, pulmonary and systemic vascular resistance, and cardiac output. These last two indexes may be misleading, however, in cases of West zones 2 or 1 and tricuspid regurgitation associated with RV dilatation. Transpulmonary thermodilution may be useful to evaluate extravascular lung water and the pulmonary vascular permeability index. To ensure adequate intravascular volume is the first goal of hemodynamic support in patients with shock. The benefit and risk balance of fluid expansion has to be carefully evaluated since it may improve systemic perfusion but also may decrease ventilator-free days, increase pulmonary edema, and promote RV failure. ACP can be prevented or treated by applying RV protective MV (low driving pressure, limited hypercapnia, PEEP adapted to lung recruitability) and by prone positioning. In cases of shock that do not respond to intravascular fluid administration, norepinephrine infusion and vasodilators inhalation may improve RV function. Extracorporeal membrane oxygenation (ECMO) has the potential to be the cause of, as well as a remedy for, hemodynamic problems. Continuous thermodilution-based and pulse contour analysis-based cardiac output monitoring are not recommended in patients treated with ECMO, since the results are frequently inaccurate. Extracorporeal CO2 removal, which could have the capability to reduce hypercapnia/acidosis-induced ACP, cannot currently be recommended because of the lack of sufficient data.

Transpulmonary pressure and lung elastance can be estimated by a PEEP-step manoeuvre.

Transpulmonary pressure is a key factor for protective ventilation. This requires measurements of oesophageal pressure that is rarely used clinically. A simple method may be found, if it could be shown that tidal and positive end-expiratory pressure (PEEP) inflation of the lungs with the same volume increases transpulmonary pressure equally. The aim of the present study was to compare tidal and PEEP inflation of the respiratory system. A total of 12 patients with acute respiratory failure were subjected to PEEP trials of 0-4-8-12-16 cmH2O. Changes in end-expiratory lung volume (ΔEELV) following a PEEP step were determined from cumulative differences in inspiratory-expiratory tidal volumes. Oesophageal pressure was measured with a balloon catheter. Following a PEEP increase from 0 to 16 cmH2O end-expiratory oesophageal pressure did not increase (0.5 ± 4.0 cmH2O). Average increase in EELV following a PEEP step of 4 cmH2O was 230 ± 132 ml. The increase in EELV was related to the change in PEEP divided by lung elastance (El) derived from oesophageal pressure as ΔPEEP/El. There was a good correlation between transpulmonary pressure by oesophageal pressure and transpulmonary pressure based on El determined as ΔPEEP/ΔEELV, r(2) = 0.80, y = 0.96x, mean bias -0.4 ± 3.0 cmH2 O with limits of agreement from 5.4 to -6.2 cmH2O (2 standard deviations). PEEP inflation of the respiratory system is extremely slow, and allows the chest wall complex, especially the abdomen, to yield and adapt to intrusion of the diaphragm. As a consequence a change in transpulmonary pressure is equal to the change in PEEP and transpulmonary pressure can be determined without oesophageal pressure measurements.

Changes in transpulmonary pressure during mechanical ventilation in patients on prolonged jackknife position: a physiological preliminary study

Changes in transpulmonary pressure during mechanical ventilation in patients on prolonged jackknife position: a physiological preliminary study

N‐butylscopolammonium bromide causes fewer side effects than atropine when assessing bronchoconstriction reversibility in horses with heaves

Bronchospasm results in airway obstruction in horses with heaves. Atropine is the most potent bronchodilator drug currently available for horses, but is associated with side effects that limit its use. Like atropine, N-butylscopolammonium bromide (NBB) is an anticholinergic agent with bronchodilatory properties. To compare the bronchodilating effects and side effects of atropine and NBB in horses with heaves. Cross-over experiment using horses with heaves. Eight horses with heaves were administered atropine and NBB, using a cross-over design. Heart rate, pupillary dilatation, transrectal palpation, lung mechanics (maximal changes in transpulmonary pressure, pulmonary resistance and elastance) and arterial blood gases were assessed before and 10 and 30 min after drug administration. One horse treated with atropine developed colic. Significant pupillary dilatation was observed only with atropine. Tachycardia developed in all horses, but was more marked with atropine. Lung function improved with both drugs, but elastance values had returned to baseline at 30 min with NBB. There was no improvement in arterial hypoxaemia with either drug. The study indicated that the bronchodilatory properties of NBB were not statistically different from those of atropine, but were of shorter duration. N-butylscopolammonium bromide was associated with fewer systemic side effects, and therefore NBB should be preferred over atropine when assessing the reversibility of airway obstruction in horses.

Experimental model to evaluate the effect of hydrothorax and lobar resection on lung compliance†

The objective of this study was to evaluate to what extent lung compliance is affected by the individual and combined action of lung resection and hydrothorax in an animal model. Anaesthetized and mechanically ventilated rabbits (weight range 2 ÷ 2.2 kg) were randomized in two groups: (i) experimental hydrothorax (from 2 to 8 ml) (n = 5) and (ii) right lower lobe lobectomy (n = 4) and right middle plus lower lobe resection (n = 2). To obtain lung compliance, we measured alveolar, oesophageal pressures and lung volume during slow inflation manoeuvres in control conditions and after hydrothorax or lung resection. Lung compliance was estimated as the change in lung volume divided by the change in transpulmonary pressure. Based on the changes in compliance of the whole lung, we calculated the corresponding changes in compliance of the right lung, which was directly exposed to unilateral hydrothorax and lobectomy. Average total lung compliance in the control was 3.3 ± 0.8 (SD) ml/cmH2O. Eight millilitres of hydrothorax significantly decreased (P < 0.001) lung compliance to 2.7 ± 0.7 ml/cmH2O and increased pleural liquid pressure at the bottom of the cavity from -1 cmH2O up to ∼ 2.5-3 cmH2O. Resection of the right lower lobe significantly decreased (P < 0.001) lung compliance to 1.75 ± 0.3 ml/cmH2O. Resection of the right middle plus lower lobes significantly decreased (P < 0.001) lung compliance to 1.52 ± 0.4 ml/cmH2O. Following hydrothorax, the decrease in right lung compliance (∼ 45%) was much greater than that expected based on the estimated decrease in right lung volume (20%). We attribute this difference to the fact that hydrothorax causes the lung to be exposed to positive, rather than sub-atmospheric, pressure, causing atelectasis. Following lobectomy, right lung compliance decreased by 62 and 80% for estimated decreases in lung volume of 30 and 60%. This difference could reflect inaccuracy in the estimate of lung volume reduction based on resected weight and/or surgical damage. We conclude that potential detrimental effects of hydrothorax and lobar resection decrease lung compliance and expose the lung to the risk of over-distension when a chest drain is applied.