Chest Wall Compliance Research Articles

CAN THEORETICAL VALUES FOR CHEST WALL COMPLIANCE BE USED IN ARDS PATIENTS?

To understand the impact of respiratory mechanics during mechanical ventilation, it is helpful to partition between the lungs and the chest wall. Esophageal pressure (Pes) is used to calculate chest wall compliance. However, esophageal pressure is not always used in the clinical arena. The value of chest wall compliance has been proposed to be estimated using 4% of the predicted value of vital capacity (VC) [1].

Anaesthetic management of a patient with Jarcho-Levin syndrome.

Anaesthetic management of a patient with Jarcho-Levin syndrome.

Elevated positive end-expiratory pressure decreases cardiac index in a rhesus monkey model.

Rationale: Clinicians are often concerned that higher positive end-expiratory pressure (PEEP) will decrease cardiac index (CI). PEEP affects CI through multiple inter-related mechanisms. The adult Rhesus monkey is an excellent model to study cardiopulmonary interaction due to similar pulmonary and chest wall compliances to human infants.Objective: Our goal was to examine the impact of increasing PEEP on CI in Rhesus monkeys as a model for critically ill children.Methods: Prospective, experimental animal study. Nine healthy anesthetized, intubated Rhesus monkeys were allowed to breathe spontaneously at a PEEP of 0, 5, 10, and 15 cm H2O while CI was measured with an ultrasonic Doppler (USCOM).Measurements and main results: Cardiac index decreased between PEEP levels of 5 and 15 cm H2O. The mean decrease in CI for the entire cohort of monkeys was 18% (p < 0.01) with a range of −11 to 49%. Stroke volume and oxygen delivery also decreased between PEEP levels of 5 and 15 cm H2O (p < 0.01).Conclusion: Between PEEP levels of 5 and 15 cm H2O, there was a decrease in CI, stroke volume, and oxygen delivery in intubated Rhesus monkeys. A plausible mechanism is that over-distention of normally compliant lungs at increased PEEP resulted in decreased preload to the right ventricle, outweighing the potentially beneficial decrease in left ventricular afterload or pulmonary vascular resistance. Further investigation is warranted, particularly in children with lung injury, who have historically benefited from increased PEEP levels without over-distention.

Inspiratory muscle training in patients with Amyotrophic Lateral Sclerosis: A systematic review.

Amyotrophic Lateral Sclerosis is a neurodegenerative disease with rapid involvement of the inspiratory muscles, leading to respiratory insufficiency. Death often occurs by aspiration and pneumonia. Endurance- and strength therapy within ALS are discussed controversially. To review the current literature to assess the efficacy of inspiratory muscle training for ALS. Systematic review, using databases as PubMed, PEDro, Cochrane and Google Scholar. Inspiratory muscle training vs. sham training or inspiratory muscle training alone. Inspiratory muscle strength, dyspnoea, quality of life and survival time. Four studies could be included in this review, two RCT's, one pre-experimental study and one with a historical control group. In total 73 patients underwent inspiratory muscle training. Studies varied in onset of the training, the training protocol and the outcomes measured. At time, there is limited evidence that inspiratory muscle training leads to strengthening of inspiratory muscles in ALS. Improvements made were minor, in only a few parameters and also in control groups. Survival time was significantly longer in the experimental group in one study. Interesting suppositions (diaphragm training vs. other IM training, improvement of chest wall and lung compliance) need to be examined in robustly designed future trials, defining exact therapeutic windows and interventions.

Inflation and deflation pressure-volume loops in anesthetized pinnipeds confirms compliant chest and lungs

We examined structural properties of the marine mammal respiratory system, and tested Scholander's hypothesis that the chest is highly compliant by measuring the mechanical properties of the respiratory system in five species of pinniped under anesthesia (Pacific harbor seal, Phoca vitulina; northern elephant seal, Mirounga angustirostris; northern fur seal Callorhinus ursinus; California sea lion, Zalophus californianus; and Steller sea lion, Eumetopias jubatus). We found that the chest wall compliance (CCW) of all five species was greater than lung compliance (airways and alveoli, CL) as predicted by Scholander, which suggests that the chest provides little protection against alveolar collapse or lung squeeze. We also found that specific respiratory compliance was significantly greater in wild animals than in animals raised in an aquatic facility. While differences in ages between the two groups may affect this incidental finding, it is also possible that lung conditioning in free-living animals may increase pulmonary compliance and reduce the risk of lung squeeze during diving. Overall, our data indicate that compliance of excised pinniped lungs provide a good estimate of total respiratory compliance.

Mechanical ventilation-induced intrathoracic pressure distribution and heart-lung interactions*.

Mechanical ventilation causes cyclic changes in the heart's preload and afterload, thereby influencing the circulation. However, our understanding of the exact physiology of this cardiopulmonary interaction is limited. We aimed to thoroughly determine airway pressure distribution, how this is influenced by tidal volume and chest compliance, and its interaction with the circulation in humans during mechanical ventilation. Intervention study. ICU of a university hospital. Twenty mechanically ventilated patients following coronary artery bypass grafting surgery. Patients were monitored during controlled mechanical ventilation at tidal volumes of 4, 6, 8, and 10 mL/kg with normal and decreased chest compliance (by elastic binding of the thorax). Central venous pressure, airway pressure, pericardial pressure, and pleural pressure; pulse pressure variations, systolic pressure variations, and stroke volume variations; and cardiac output were obtained during controlled mechanical ventilation at tidal volume of 4, 6, 8, and 10 mL/kg with normal and decreased chest compliance. With increasing tidal volume (4, 6, 8, and 10 mL/kg), the change in intrathoracic pressures increased linearly with 0.9 ± 0.2, 0.5 ± 0.3, 0.3 ± 0.1, and 0.3 ± 0.1 mm Hg/mL/kg for airway pressure, pleural pressure, pericardial pressure, and central venous pressure, respectively. At 8 mL/kg, a decrease in chest compliance (from 0.12 ± 0.07 to 0.09 ± 0.03 L/cm H2O) resulted in an increase in change in airway pressure, change in pleural pressure, change in pericardial pressure, and change in central venous pressure of 1.1 ± 0.7, 1.1 ± 0.8, 0.7 ± 0.4, and 0.8 ± 0.4 mm Hg, respectively. Furthermore, increased tidal volume and decreased chest compliance decreased stroke volume and increased arterial pressure variations. Transmural pressure of the superior vena cava decreased during inspiration, whereas the transmural pressure of the right atrium did not change. Increased tidal volume and decreased chest wall compliance both increase the change in intrathoracic pressures and the value of the dynamic indices during mechanical ventilation. Additionally, the transmural pressure of the vena cava is decreased, whereas the transmural pressure of the right atrium is not changed.

Rabbit model of chest wall rigidity induced by fentanyl and the effects of apomorphine

A rabbit model for fentanyl-induced chest wall rigidity and the effect of apomorphine was evaluated. Eleven New Zealand adult rabbits were anesthetized and mechanically ventilated. An esophageal balloon catheter was used to estimate pleural pressure (Ppl). Chest wall compliance (Ccw) at baseline was calculated during pentobarbital anesthesia. A loading dose of 0.1mgkg−1 of fentanyl followed by infusion of 0.01mgkg−1min−1 was started in all animals, and Ccw reassessed. In the rabbits that developed decreased Ccw, apomorphine 0.4mgkg−1 followed by a 0.004mgkg−1min−1 was administered and Ccw was reassessed. Ccw at baseline and after fentanyl and fentanyl+apomorphine were compared with one-way ANOVA followed by Bonferroni–Holm test (P<0.05). In 5 rabbits, Ccw decreased significantly after fentanyl administration and apomorphine was able to restore Ccw to baseline values. Rabbits can be used as a model for fentanyl-induced chest wall rigidity. Results from this study support central dopaminergic pathways as being at least partially responsible for the opioid-induced chest wall rigidity.

Effects of breast reduction on pulmonary function.

Macromastia causes several health problems, and reduction surgery alleviates them successfully. The purpose of this study was to investigate whether reduction mammaplasty improves possible impairments on pulmonary functions related to macromastia. Thirty-one patients participated in the study. Pulmonary function tests were performed before and 3 months after surgery with a spirometry. Preoperative and postoperative pulmonary function values were compared using a paired t test. Two patients were found to have mild restriction in preoperative spirometric analysis, and they went to normal range in postoperative analysis. All other patients were assessed as having normal values in both preoperative and postoperative analyses. Preoperative and postoperative forced vital capacity values were 2.72±0.06 and 2.79±0.05 L, respectively. The difference was statistically significant (paired t test, P=0.014). The other parameter in which breast reduction had statistically significant improvement was forced vital capacity performed/predicted ratio (paired t test, P=0.041). Additionally, the weight of resected breast tissue correlated significantly with the change of forced vital capacity (Pearson correlation coefficient=0.379, P=0.036). Breast reduction surgery improves the pulmonary function parameters that are mainly influenced by restrictive states. This result led us to consider that macromastia causes a relative restriction in chest wall compliance, and reduction of breast weight may enhance chest wall compliance and improve pulmonary function.

Diagnosis and management of patients with pleural effusions.

Pleural effusions occur when fluid accumulates between the visceral and parietal pleura in the chest cavity, preventing the lung from expanding fully during inspiration. The reduction in lung volume, depression of the diaphragm and reduced chest wall compliance cause dyspnoea, and occasionally pain or cough. Pleural effusion is a complex problem caused by a variety of conditions requiring different treatment depending on the underlying diagnosis. This article discusses the causes and treatment of pleural effusions, referencing guidelines produced by the British Thoracic Society.

Lung Volumes and Their Significance for Pharyngeal and Esophageal Swallowing Function

Subglottic airway pressure is generated during each swallow and this supports the probability that subglottic mechanoreceptors function as part of the overall afferent collage of signals that guide motor output. Lung volume at swallow onset, lung recoil forces, and chest wall compliance are all important factors that combine for the generation of sufficiently positive subglottic air pressure during the pharyngeal swallow. Higher lung volumes at swallow onset may also be advantageous to the esophageal pressure gradient during esophageal bolus transit. Patients with impaired lung-thoracic unit recoil and disordered breathing/swallowing patterns may not only benefit from learning to swallow during early exhalation, but may also need to start at a higher lung volume in order to compensate for reduced recoil effects on swallowing function.

Drainage of pleural effusion in mechanically ventilated patients: Time to measure chest wall compliance?

PurposePleural effusion (PE) is commonly encountered in mechanically ventilated, critically ill patients and is generally addressed with evacuation or by fluid displacement using increased airway pressure (PAW). However, except when massive or infected, clear evidence is lacking to guide its management. The aim of this study was to investigate the effect of recruitment maneuvers and drainage of unilateral PE on respiratory mechanics, gas exchange, and lung volume. Materials and methodsFifteen critically ill and mechanically ventilated patients with unilateral PE were enrolled. A 3-step protocol (baseline, recruitment, and effusion drainage) was applied to patients with more than 400 mL of PE, as estimated by chest ultrasound. Predefined subgroup analysis compared patients with normal vs reduced chest wall compliance (CCW). Esophageal and PAWs, respiratory system, lung and CCWs, arterial blood gases, and end-expiratory lung volumes were recorded. ResultsIn the whole case mix, neither recruitment nor drainage improved gas exchange, lung volume, or tidal mechanics. When CCW was normal, recruitment improved lung compliance (81.9 [64.8-104.1] vs 103.7 [91.5-111.7] mL/cm H2O, P < .05), whereas drainage had no significant effect on total respiratory system mechanics or gas exchange, although it measurably increased lung volume (1717 vs 2150 mL, P < .05). In the setting of reduced CCW, however, recruitment had no significant effect on total respiratory system mechanics or gas exchange, whereas pleural drainage improved respiratory system and CCWs as well as lung volume (42.7 [38.9-50.0] vs 47.0 [43.8-63.3], P < .05 and 97.4 [89.3-97.9] vs 126.7 [92.3-153.8] mL/cm H2O, P < .05 and 1580 vs 1750 mL, P < .05, respectively). ConclusionsDrainage of a moderate-sized effusion should not be routinely performed in unselected population of critically ill patients. We suggest that measurement of CCW may help in the decision-making process.

(827) - Prevalence of Forgut Dysfunction in Pulmonary Fibrosis and COPD Patients Undergoing LTx Evaluation

Pulmonary fibrosis (PF) & COPD are progressive and fatal lung diseases that lead to lung transplantation (LTx). However, the respiratory physiology, intrathoracic pressure variation, and chest wall compliance are markedly different. Gastroesophageal reflux (GER) is a significant risk factor for development and/or progression of end-stage lung disease pre-LTx and chronic rejection post-LTx. This study attempts to define the prevalence of forgut dysfunction based on comprehensive GI testing in patients with end-stage PF and COPD undergoing transplant evaluation. From February 2009-March 2012 126 people underwent bilateral lung transplantation. These patients underwent comprehensive pre-transplant GER work-up including EGD, manometry, esophagram pH testing and nuclear medicine gastric emptying studies. Except gastric emptying readings, all foregut function studies were performed by the same transplant surgeons. Tests were analyzed for comparison between groups according to disease states. The association for group by outcome variables were tested using contingency tables and a chi-square test statistics. Complete data was collected in 82 patients with a mean age of 56.5 years +/- 14.4 years. 41(50%) classified as COPD, 41(50%) PF. No significant differences in prevalence of hiatal hernia (HH) (46% vs. 64%), barrett’s (3% vs. 0%) or delayed gastric emptying (17% vs. 13%) between COPD vs. PF respectively. Similarly, no difference noted in manometer LES basal tone and wave amp @ 7cm. Mean DeMeester pH scores significantly higher in PF (40.1) vs. COPD (15.5), p=0.003. Proportion of time with pH < 4 was significantly higher in PF vs. COPD (1.5% vs. 0.5%, p=0.015). The prevalence of forgut dysfunction based on comprehensive GI testing in patients with end-stage lung disease is significant. pH probe assessment demonstrated a significantly higher proportion of time spent at pH< 4 and elevated DeMeester scores in PF compared to COPD. However, no significant difference were noted in the presence of HH or barrett’s, delayed gastric emptying, or manometer assessments between cohorts.

Positive end-expiratory pressure adjustment in parenchimal respiratory failure: static pressure-volume loop or transpulmonary pressure?

The aim of the study was compare the prognostic value, efficacy and safety ofpositive end-expiratory pressure (PEEP) adjustment in conformity with lower inflection point of static "pressure-volume" loop (LIP) or end-expiratory esophageal pressure (EEEP) in parenchymal respiratory failure. We included in the study 56 patients (39 males) at age 47 +/- 17.8 years with parenchymal respiratory failure (PaO2/FiO2 < 250 mmHg, bilateral infiltrates on chest X-ray or lung CT scan, no signs of left ventricular failure), who were mecAanically ventilated for less than 48 hours. All patients were sedated and paralyzed. We measured intra- Sabdominal pressure, PaO2/FiO2, PaCO2, alveolar dead space (Vdalv), plotted static "pressure-volume" loop by low flow technique in range of 0 to 40 mbar, recording LIP Then we placed nasogastric tube with balloon for esophageal pressure measurement and measured esophageal pressure at PEEP range from 8 to 20 mbar (with 2 mbar steps) and recorded plateau pressure (Pplat), transpulmonary plateau pressure (Ptp plat), transpulmonary pressure at PEEP level (Ptp PEEP), static compliance of respiratory system (Cstat), lung compliance (Clung), chest wall compliance (Ccw) at every step. Also by volumetric capnography technique we measured end-tidal carbon dioxide concentration (EtCO2), minute volume of exhaled carbon dioxide (VCO2) volume of exhaled carbon dioxide by single breath (VtCO2) and calculate VC2/EtCO2 as a surrogate marker of pulmnonary perfusion. After that we set PEEP at EEEP level (at zero end-expirato- my ranspulmonary pressure) and recorded changes of PaO2/FiO2 and Vdalv. LIP value was 5 (6-10) mbar and it was less than empirically set PEEP in most of patients before enrollment and had no prognostic value for PEEP setting. EEEP level was 14 (12-18.25) mbar and it was higher than LIP in 96.4% patients. Distribution of EEEP values was close to normal unlike LIP Chest wall compliance was less than normal (100 ml/mbar) in 46% of patients. EEEP has correlation with body mass index (rho 0.554, p=0.002). We did not find any correlation between intra-abdominal pres- sure (IAP) and EEEP (p=0.376) or IAP and LIP (p=0.464). PEEP levels higher than 14 mbar led to significant decrease in Cstat and Clung (p<0.001). We observed significant decrease in VCO at PEEP levels more than 16 mbar, i.e., more than EEEP median. PEEP levels more than 16 mbar decreased VCO2/EtCO2, (decreased pulmonary perfusion) from 7.47 (6.54-8.7) at PEEP 14 mbar to 7.32 (6.35-8.76) at PEEP 20 mbar (p=0.004). PEEP setting at EEEP level increased PaO/FiO2 from 205 (154-235) to 280 (208-358) mmHg (p<0.001), did hot change Vdalv (p=0.093) and decreased Cstat and Clung in the most of patients (64.3%). L1P was lower than empirically set PEEP in most patients and did not help to optimize gas exchange. PEEP setting at EEEP level in patients with parenchimal respiratory failure increases PaO/FiO, (reflects opening of collapsed alveoli), decreases volume of expired carbon dioxide and decreases lung compliance (reflects overdistenion of opened alveoli). VCO2/EtCO2 ratio decreases (decreased pulmonary perfusion) at PEEP levels more than 16 mbar, which was more than EEEP.

Pressure controlled vs. volume controlled ventilation during prone position in high-level spinal cord injury patients: a preliminary study.

Pressure controlled vs. volume controlled ventilation during prone position in high-level spinal cord injury patients: a preliminary study.

Positive end expiratory pressure titrated by transpulmonary pressure improved oxygenation and respiratory mechanics in acute respiratory distress syndrome patients with intra-abdominal hypertension

Background Intra-abdominal hypertension (IAH) is common in acute respiratory distress syndrome (ARDS) patients and when resulting in decrease of chest wall compliance will weaken the effect of positive end expiratory pressure (PEEP). We investigated the effect of PEEP titrated by transpulmonary pressure (Ptp) on oxygenation and respiratory mechanics in ARDS patients with IAH compared with PEEP titrated by ARDSnet protocol. Methods ARDS patients admitted to the intensive care unit (ICU) of the Zhongda Hospital were enrolled. Patients were ventilated with volume control mode with tidal volume of 6 ml/kg under two different PEEP levels titrated by Ptp method and ARDSnet protocol. Respiratory mechanics, gas exchange and haemodynamics were measured after 30 minutes of ventilation in each round. IAH was defined as intra-abdominal pressure of 12 mmHg or more. Results Seven ARDS patients with IAH and 8 ARDS patients without IAH were enrolled. PEEP titrated by Ptp were significant higher than PEEP titrated by ARDSnet protocol in both ARDS patients with IAH ((17.3±2.6) cmH2O vs. (6.3±1.6) cmH2O and without IAH ((9.5±2.1) cmH2O vs. (7.8±1.9) cmH2O). Arterial pressure of O2/fraction of inspired oxygen (PaO2/FiO2) was much higher under PEEP titrated by Ptp when compared with PEEP titrated by ARDSnet protocol in ARDS patients with IAH ((27.2±4.0) cmHg vs. (20.9± 5.0) cmHg. But no significant difference of PaO2/FiO2 between the two methods was found in ARDS patients without IAH. In ARDS patients with IAH, static compliance of lung and respiratory system were higher under PEEP titrated by Ptp than by ARDSnet protocol. In ARDS patients with IAH, central venous pressure (CVP) was higher during PEEP titrated by Ptp than by ARDSnet protocol. Conclusion Positive end expiratory pressure titrated by transpulmonary pressure was higher than PEEP titrated by ARDSnet protocol and improved oxygenation and respiratory mechanics in ARDS patients with IAH.

Sugammadex to rescue a ‘can't ventilate’ scenario in an anticipated difficult intubation: is it the answer?

Sugammadex to rescue a ‘can't ventilate’ scenario in an anticipated difficult intubation: is it the answer?

Endoscopic Ultrasound-Guided Therapeutic Thoracentesis

Diagnostic or therapeutic thoracentesis in patients with mechanical ventilation is typically performed with ultrasound guidance using a posterolateral approach.1 Recently, the use of endoscopic ultrasound (EUS) for detection and aspiration of pleural effusions2,3 and the feasibility of bedside EUS in critically ill patients has been described.4,5 We present a case of EUS-guided therapeutic thoracentesis performed at the bedside in a critically ill patient on mechanical ventilation. A 69-year-old female was admitted to our hospital with acute liver failure suspected to be secondary to drug toxicity. She was transferred to the intensive care unit because of worsening liver failure, hepatic encephalopathy, atrial fibrillation, fluid overload, and respiratory distress requiring intubation. Chest radiography (Fig. 1) and abdominal computed tomography revealed a large right pleural effusion, pancreatic mass and possible cirrhosis. She was not deemed a candidate for an urgent liver transplant because of the indeterminate pancreatic mass. Furthermore, systemic chemotherapy and radiation were not considered because of acute liver failure. Bedside EUS was requested by the intensive care unit team for both tissue diagnosis of the pancreatic mass and therapeutic thoracentesis to facilitate ventilation. Endoscopy was performed in a supine position while the patient was on mechanical ventilation. EUS revealed a 25×20 mm T2NxMx solid and cystic mass in the pancreatic body (Fig. 2), and fine needle aspiration (FNA) using a 22-gauge needle with on-site cytology review was consistent with adenocarcinoma. Therapeutic thoracentesis of the right-sided pleural effusion was then performed. The stylet was removed from a 19-gauge needle (Echotip; Wilson-Cook Endoscopy, Winston-Salem, NC, USA), and transesophageal puncture of the right pleural space was performed (Fig. 3). Fluid was removed by attaching tubing between the proximal end of the needle and a suction canister. A total of 2 L was removed without complications over a 30-minute period. The total procedure time was 70 minutes. Cytology from the pleural fluid was negative for malignancy, and the fluid was transudative. Hypoxemia improved following the procedure, and follow-up chest radiography showed no pneumothorax or worsening pulmonary edema. The patient's family was informed of the diagnosis of pancreatic malignancy. Based on the patient's previous written wishes, the confirmed diagnosis of malignancy and the liver failure, medical care was withdrawn 24 hours later, and the patient expired. Fig. 1 Large right pleural effusion observed using chest radiograph. Fig. 2 Solid and cystic mass in the pancreatic body. Fig. 3 Aspiration of right pleural space with 22-gauge needle. To our knowledge, this case represents the first report of EUS-guided therapeutic thoracentesis performed at the bedside in a critically ill patient on mechanical ventilation. Currently, there are limited data on the utility of EUS for thoracentesis3 and bedside EUS.4,5 Furthermore, only one case of EUS-guided therapeutic paracentesis has been described.6 EUS-FNA of pancreatic cyst fluid is traditionally performed using a 22- or 25-gauge needle with a 10-mL syringe attached to the proximal end for suction. Aspiration of large volumes of fluid using such a small needle and syringe would be time-consuming and impractical. Using a 19-gauge FNA needle attached to continuous suction, we were able to perform large-volume therapeutic thoracentesis in a fashion similar to that described in a previous report of EUS-guided therapeutic paracentesis.6 Thoracentesis was requested in our patient only because simultaneous EUS-FNA of a pancreatic mass was necessary. As percutaneous ultrasound-guided thoracentesis in patients on mechanical ventilation has been shown to be feasible and safe in patients without significant coagulopathy,1,7-9 we believe that EUS guidance should be considered only in cases in which EUS is required for another reason. Pleural effusions are commonly recognized in critically ill patients, and their management remains poorly standardized.9 Commonly cited reasons for drainage include diagnosis of infection, hypoxemia, excessive ventilator pressure or difficulty in weaning from mechanical ventilation. With the exception of established infection of the pleural space, the balance of risk and benefit of pleural drainage remains fairly controversial for each of these indications.9 Pleural drainage may improve hypoxemia or lung mechanics, but the physiological response depends on a complex interplay among lung and chest-wall compliance, applied positive expiratory pressure and drainage volume.9 In conclusion, EUS-guided therapeutic thoracentesis is feasible and may be considered when EUS is required for another indication or when the traditional posterior approach is not feasible.

In Reply:

The authors sincerely thank Dr. Roth for his letter regarding their recent article1 and are happy to respond to his comments and anecdotes.The problematic of chest wall compliance is of interest and is not new. In 1989, Pizov et al.2 demonstrated in a canine model that reducing chest wall compliance by external chest compression induced an increase in the deltadown component of the systolic pressure variation, suggesting a decrease in the venous return. More recently, Mesquida et al.3 found an increase in pulse pressure variations and stroke volume variations after reduction in chest wall compliance induced by chest and abdominal binders in an experimental study. As suggested by Dr. Roth, decrease in chest wall compliance may be due to truncal rigidity. This situation may be related to a lack of sedation (which contraindicates the use of dynamic indices) or may be provoked by high doses of opioids (an uncommon practice actually even in cardiac surgery). In contrast, a decrease in chest wall compliance secondary to abdominal hypertension is a common situation in an operating room (laparoscopy) or an intensive care unit. As highlighted in the article, abdominal hypertension may lead to an increase in pulse pressure variations in this setting.1To our knowledge, the ability of dynamic index to predict fluid responsiveness in the specific obese population has not yet been tested. The possible impact of obesity should be more complex than stated by Dr. Roth. Indeed, a direct effect of the fat distribution in obese patients is a reduction in the respiratory system compliance due to the reduction in lung and chest wall compliance.4,5 As mentioned previously, decrease in chest wall compliance will induce an increase in pulse pressure variations. In contrast, during decreased lung compliance, airway pressure transmission is reduced such that the cyclic changes in intrathoracic pressure could be attenuated even in case of marked changes in alveolar pressure.6 Thus, Monnet et al.7 recently demonstrated that the predictive value of pulse pressure variations is related to lung compliance. The clinical impact of these hypothetic mechanisms, which is probably low, except for morbid obese patients, remains to be demonstrated.We do not agree with Dr. Roth when he claims that administering neuromuscular blockade may result in a lower volume infusion. This affirmation is not supported by any publication. The impact of neuromuscular blockade administered in anesthetized patients without pathological decrease in chest wall compliance on dynamic index has never been demonstrated. Furthermore, most of the patients included in validation studies of dynamic index in intensive care unit were not paralyzed.8On the contrary, we totally agree with Dr. Roth that stroke volume variations and its surrogates should not be the endpoint of therapy. As clearly mentioned in the article, the dynamic index must be considered as useful tools to predict an increase in stroke volume after volume expansion. But they clearly cannot help to answer the following question: Does my patient need an increase in stroke volume?

Intraoperative plateau pressure measurement using modern anesthesia machine ventilators

Monitoring respiratory system mechanics is vital to guide safe and effective ventilator management. Transalveolar pressure (tAp) is the driving force of alveolar distension, which allows for effective respiration; however, overdistension may lead to inflammation and subsequent destruction of alveoli. Unfortunately, there is no practical way to measure tAp directly; hence, surrogate measures are often used. Peak airway pressure (PAP), commonly monitored in patients undergoing general anesthesia, consists of static and dynamic components. Volume-preset ventilation allows determination of the respiratory system mechanics. In a muscle-relaxed patient, PAP consists of two components, i.e., the dynamic pressure to drive gas across the resistance (Pres) of the bronchial tree and the static pressure to expand the alveoli against the elastic recoil of the lungs and chest wall (Plateau pressure, [Pplat]), which is more reflective of tAp than PAP. Plateau pressure can be displayed easily on the new generation of anesthesia machine ventilators by inserting an end-inspiratory pause of 0.5-1 sec. Calculating the difference in airway pressure during flow and no-flow states allows the calculation of airway resistance (Pres = PAP Pplat). Diagnostic and therapeutic information can be extracted by distinguishing components of PAP. This information can help the anesthesia provider to narrow the differential diagnosis of high PAP to help solve oxygenation/ventilation issues and tailor treatment. For example, elevated Pres at constant flow may indicate bronchospasm or endotracheal tube obstruction (Figure). Conversely, falling Pres may correspond with a response to bronchodilators. Elevated Pplat indicates excessive tidal volume or decreased lung and/or chest wall compliance (e.g., pulmonary edema, acute lung injury, or abdominal distension). Positive pressure ventilation may cause or exacerbate lung injury due to an increase in lung stretching which is best assessed by the transpulmonary pressure or the tAp. Separation of lungs from chest wall compliance requires an esophageal pressure measurement to approximate pleural pressure. Due to the technical and accuracy limitations, esophageal manometry is not widely used, and Pplat is used as a surrogate to guide titration of mechanical ventilation. As a lung protective ventilation strategy, it is recommended that Pplat be maintained B 30 cm H2O to prevent alveolar overdistension and barotrauma, especially in acute lung injury and during one-lung ventilation. Whenever chest compliance is reduced, the stiff chest contributes substantially to Pplat. This should be taken into consideration when assessing lung stretch, as higher Pplat may still be safe due to the limitation of alveolar distension by the chest wall. We present two examples of procedures to acquire Pplat in the operating room using two popular anesthesia machines. For the GE S/5 Aespire SmartVent (General Electric Company, Madison, WI, USA) (Figure), select setup/calibration from the main menu (Figure, upper panel); then change the inspiratory pause from 0 to 30-60% to achieve a pause of 0.5-1 sec, and Pplat will be displayed (Figure, lower panel). With a respiratory rate of 8 breaths min and inspiratory:expiratory (I:E) ratio 1:2, M. A. Helwani, MD (&) Washington University School of Medicine, St. Louis, MO, USA e-mail: helwanim@anest.wustl.edu

Systemic leptin produces a long-lasting increase in respiratory motor output in rats

Leptin decreases food intake and increases energy expenditure. Leptin administration into the CNS of mice or rats increases alveolar ventilation and dysfunction in leptin signaling has been implicated in the hypoventilation that can accompany obesity. An increase in CO2 chemosensitivity has been implicated in this response but it is unclear whether ventilation is augmented when PCO2 is maintained constant. We examined the effects of intravenous leptin to test the hypothesis that systemic leptin administration in isoflurane anesthetized, mechanically ventilated and vagotomized rats would lead to a sustained increase in respiratory motor output that was independent of changes in end-tidal PCO2, body temperature or lung inflation pressure (an indicator of overall lung and chest wall compliance). In anesthetized Sprague-Dawley rats with end-tidal PCO2, lung compliance and rectal temperature maintained constant, injection of a bolus of leptin (0.25 mg, 0.5 mg/ml, i.v.), followed over the next 1 h by the intravenous infusion of an additional 0.25 mg, elicited a progressive increase in the peak amplitude of integrated phrenic nerve discharge lasting at least 1 h beyond the end of the infusion. The increase peaked at 90 min at 58.3 ± 5.7% above baseline. There was an associated increase in the slope of the phrenic response to increasing inspired CO2. There was also a moderate and sustained decrease in arterial pressure 9 ± 1.3 mmHg at 120 min, with no associated change in heart rate. These data indicate that leptin elicits a sustained increase in respiratory motor output that outlasts the administration leptin via a mechanism that does not require alterations in arterial PCO2, body temperature, or systemic afferent feedback via the vagus nerves. This stimulation may help to prevent obesity-related hypoventilation.