Amal Jubran

The application of esophageal pressure measurement in patients with respiratory failure.

This report summarizes current physiological and technical knowledge on esophageal pressure (Pes) measurements in patients receiving mechanical ventilation. The respiratory changes in Pes are representative of changes in pleural pressure. The difference between airway pressure (Paw) and Pes is a valid estimate of transpulmonary pressure. Pes helps determine what fraction of Paw is applied to overcome lung and chest wall elastance. Pes is usually measured via a catheter with an air-filled thin-walled latex balloon inserted nasally or orally. To validate Pes measurement, a dynamic occlusion test measures the ratio of change in Pes to change in Paw during inspiratory efforts against a closed airway. A ratio close to unity indicates that the system provides a valid measurement. Provided transpulmonary pressure is the lung-distending pressure, and that chest wall elastance may vary among individuals, a physiologically based ventilator strategy should take the transpulmonary pressure into account. For monitoring purposes, clinicians rely mostly on Paw and flow waveforms. However, these measurements may mask profound patient-ventilator asynchrony and do not allow respiratory muscle effort assessment. Pes also permits the measurement of transmural vascular pressures during both passive and active breathing. Pes measurements have enhanced our understanding of the pathophysiology of acute lung injury, patient-ventilator interaction, and weaning failure. The use of Pes for positive end-expiratory pressure titration may help improve oxygenation and compliance. Pes measurements make it feasible to individualize the level of muscle effort during mechanical ventilation and weaning. The time is now right to apply the knowledge obtained with Pes to improve the management of critically ill and ventilator-dependent patients.

Meta-analysis under the spotlight: focused on a meta-analysis of ventilator weaning.

Objective:Because the results of a meta-analysis are used to formulate the highest level recommendation in clinical practice guidelines, clinicians should be mindful of problems inherent in this technique. Rather than reviewing meta-analysis in abstract, general terms, we believe readers can gain a more concrete understanding of the problems through a detailed examination of one meta-analysis. The meta-analysis on which we focus is that conducted by an American College of Chest Physicians/American Association for Respiratory Care/American College of Critical Care Medicine Task Force on ventilator weaning. Data Source:Two authors extracted data from all studies included in the Task Force’s meta-analysis. Data Synthesis and Overview:The major obstacle to reliable internal validity and, thus, reliable external validity (generalizability) in biological research is systematic error, not random error. If systematic errors are present, averaging (as with a meta-analysis) does not decrease them—instead, it reinforces them, producing artifact. The Task Force’s meta-analysis commits several examples of the three main types of systematic error: selection bias (test-referral bias, spectrum bias), misclassification bias (categorizing reintubation as weaning failure, etc.), and confounding (pressure support treated as unassisted breathing). Several additional interpretative errors are present. Conclusions:An increase in study size, as achieved through the pooling of data in a meta-analysis, is mistakenly thought to increase external validity. On the contrary, combining heterogeneous studies poses considerable risk of systematic error, which impairs internal validity and, thus, external validity. The strength of recommendations in clinical practice guidelines is based on a misperception of the relative importance of systematic vs. random error in science.

Esophageal and transpulmonary pressure in the clinical setting: meaning, usefulness and perspectives

PurposeEsophageal pressure (Pes) is a minimally invasive advanced respiratory monitoring method with the potential to guide management of ventilation support and enhance specific diagnoses in acute respiratory failure patients. To date, the use of Pes in the clinical setting is limited, and it is often seen as a research tool only.MethodsThis is a review of the relevant technical, physiological and clinical details that support the clinical utility of Pes.ResultsAfter appropriately positioning of the esophageal balloon, Pes monitoring allows titration of controlled and assisted mechanical ventilation to achieve personalized protective settings and the desired level of patient effort from the acute phase through to weaning. Moreover, Pes monitoring permits accurate measurement of transmural vascular pressure and intrinsic positive end-expiratory pressure and facilitates detection of patient–ventilator asynchrony, thereby supporting specific diagnoses and interventions. Finally, some Pes-derived measures may also be obtained by monitoring electrical activity of the diaphragm.ConclusionsPes monitoring provides unique bedside measures for a better understanding of the pathophysiology of acute respiratory failure patients. Including Pes monitoring in the intensivist’s clinical armamentarium may enhance treatment to improve clinical outcomes.

Narrative Review: Ventilator-Induced Respiratory Muscle Weakness

Clinicians have long been aware that substantial lung injury results when mechanical ventilation imposes too much stress on the pulmonary parenchyma. Evidence is accruing that substantial injury may also result when the ventilator imposes too little stress on the respiratory muscles. Through adjustment of ventilator settings and administration of pharmacotherapy, the respiratory muscles may be rendered almost (or completely) inactive. Research in animals has shown that diaphragmatic inactivity produces severe injury and atrophy of muscle fibers. Human data have recently revealed that 18 to 69 hours of complete diaphragmatic inactivity associated with mechanical ventilation decreased the cross-sectional areas of diaphragmatic fibers by half or more. The atrophic injury seems to result from increased oxidative stress leading to activation of protein-degradation pathways. Scientific understanding of ventilator-induced respiratory muscle injury has not reached the stage where meaningful controlled trials can be done, and thus, it is not possible to give concrete recommendations for patient management. In the meantime, clinicians are advised to select ventilator settings that avoid both excessive patient effort and excessive respiratory muscle rest. The contour of the airway pressure waveform on a ventilator screen provides the most practical indication of patient effort, and clinicians are advised to pay close attention to the waveform as they titrate ventilator settings. Research on ventilator-induced respiratory muscle injury is in its infancy and portends to be an exciting area to follow.

Ventilator-induced respiratory muscle weakness

The most common reason to institute mechanical ventilation is to decrease patient distress resulting from an increase in work of breathing (1). In this situation, the ventilator is functioning as an additional set of muscles, and so decreases the load placed on the patient’s own respiratory muscles. The second major indication for mechanical ventilation is to improve oxygenation, as, for example, in patients with the acute respiratory distress syndrome (ARDS) (1). A ventilator improves oxygenation by increasing tidal volume and end-expiratory lung volume, and by better matching of ventilation and perfusion within the lung parenchyma (2). While the oxygen-enhancing action of the ventilator is not directed at the respiratory muscles per se, patients with impaired oxygenation are commonly treated with antibiotics (3), corticosteroids (4), sedatives (5) and neuromuscular agents (6), all of which can weaken respiratory muscles. Every patient who survives an episode of acute respiratory failure faces a major challenge at the point of ventilator discontinuation. The main reason that patients fail weaning attempts is because their work of breathing is high consequent to abnormal lung mechanics (increased resistance, decreased compliance) and their respiratory muscles are unable to cope with the increased load (7). From the above account, it is evident that performance of the respiratory muscles is a dominant consideration at the points when mechanical ventilation is first instituted and when it is being withdrawn. A major concern of critical care physicians is the growing awareness that mechanical ventilation can harm the lung. From the earliest days of intensive care, it has been recognized that use of high airway pressure can rupture the lung parenchyma, causing a pneumothorax. In 1974, Webb and Tierney demonstrated that mechanical ventilation can cause hemorrhagic and edematous lesions independent of barotrauma (8). This seminal observation was extended by other animal experiments and the alveolar injury has been shown to result from the use of high tidal volumes; the injury has been named volutrauma or ventilator-induced lung injury (9). Studies in animals were followed by studies in patients, which culminated in randomized controlled trials that have shown that use of high tidal volume leads to increased mortality in patients with ARDS. Just as mechanical ventilation can damage the lung parenchyma, investigators have postulated that the ventilator can damage the respiratory muscles (10). The fear is that mechanical ventilation lowers demands on a patient’s respiratory muscles to such an extent that they become inactive, resulting in injury and atrophy at a structural level. In contrast to research on ventilator-induced lung injury, scientific understanding of ventilator-induced respiratory muscle injury has not reached the stage where it is possible to undertake meaningful randomized controlled trials and thus it is not possible to render concrete recommendations for patient management. Nevertheless, the accruing biological and pathophysiological research on the effect of mechanical ventilation on the respiratory muscles is leading many experts to change their approach to ventilator management.

MONITORING DURING MECHANICAL VENTILATION

Approximately half of the patients admitted to an ICU are admitted for the purposes of monitoring rather than interventional therapy. In the last decade, significant technologic advances have enhanced monitoring capacities, and the understanding of the pathophysiology of respiratory failure has improved pari passu, allowing clinicians to employ monitors in a more intelligent manner. This article deals with new developments in arterial blood gas monitoring, pulse oximetry, capnometry, and monitoring of neuromuscular function and pulmonary mechanics, emphasizing issues most relevant to mechanical ventilation.

Ventilatory Failure, Ventilator Support, and Ventilator Weaning

The development of acute ventilatory failure represents an inability of the respiratory control system to maintain a level of respiratory motor output to cope with the metabolic demands of the body. The level of respiratory motor output is also the main determinant of the degree of respiratory distress experienced by such patients. As ventilatory failure progresses and patient distress increases, mechanical ventilation is instituted to help the respiratory muscles cope with the heightened workload. While a patient is connected to a ventilator, a physicians ability to align the rhythm of the machine with the rhythm of the patients respiratory centers becomes the primary determinant of the level of rest accorded to the respiratory muscles. Problems of alignment are manifested as failure to trigger, double triggering, an inflationary gas-flow that fails to match inspiratory demands, and an inflation phase that persists after a patients respiratory centers have switched to expiration. With recovery from disorders that precipitated the initial bout of acute ventilatory failure, attempts are made to discontinue the ventilator (weaning). About 20% of weaning attempts fail, ultimately, because the respiratory controller is unable to sustain ventilation and this failure is signaled by development of rapid shallow breathing. Substantial advances in the medical management of acute ventilatory failure that requires ventilator assistance are most likely to result from research yielding novel insights into the operation of the respiratory control system.

Validity and reliability of rectus femoris ultrasound measurements: Comparison of curved-array and linear-array transducers

Muscle-mass loss augers increased morbidity and mortality in critically ill patients. Muscle-mass loss can be assessed by wide linear-array ultrasound transducers connected to cumbersome, expensive console units. Whether cheaper, hand-carried units equipped with curved-array transducers can be used as alternatives is unknown. Accordingly, our primary aim was to investigate in 15 nondisabled subjects the validity of measurements of rectus femoris cross-sectional area by using a curved-array transducer against a linear-array transducer-the reference-standard technique. In these subjects, we also determined the reliability of measurements obtained by a novice operator versus measurements obtained by an experienced operator. Lastly, the relationship between quadriceps strength and rectus area recorded by two experienced operators with a curved-array transducer was assessed in 17 patients with chronic obstructive pulmonary disease (COPD). In nondisabled subjects, the rectus cross-sectional area measured with the curved-array transducer by the novice and experienced operators was valid (intraclass correlation coefficient [ICC]: 0.98, typical percentage error [%TE]: 3.7%) and reliable (ICC: 0.79, %TE: 9.7%). In the subjects with COPD, both reliability (ICC: 0.99) and repeatability (%TE: 7.6% and 9.8%) were high. Rectus area was related to quadriceps strength in COPD for both experienced operators (coefficient of determination: 0.67 and 0.70). In conclusion, measurements of rectus femoris cross-sectional area recorded with a curved-array transducer connected to a hand-carried unit are valid, reliable, and reproducible, leading us to contend that this technique is suitable for cross-sectional and longitudinal studies.

Diaphragmatic neuromechanical coupling and mechanisms of hypercapnia during inspiratory loading.

We hypothesized that improved diaphragmatic neuromechanical coupling during inspiratory loading is not sufficient to prevent alveolar hypoventilation and task failure, and that the latter results primarily from central-output inhibition of the diaphragm and air hunger rather than contractile fatigue. Eighteen subjects underwent progressive inspiratory loading. By task failure all developed hypercapnia. Tidal transdiaphragmatic pressure (ΔPdi) and diaphragmatic electrical activity (ΔEAdi) increased during loading - the former more than the latter; thus, neuromechanical coupling (ΔPdi/ΔEAdi) increased during loading. Progressive increase in extra-diaphragmatic muscle contribution to tidal breathing, expiratory muscle recruitment, and decreased end-expiratory lung volume contributed to improved neuromechanical coupling. At task failure, subjects experienced intolerable breathing discomfort, at which point mean ΔEAdi was 74.9±4.9% of maximum, indicating that the primary mechanism of hypercapnia was submaximal diaphragmatic recruitment. Contractile fatigue was an inconsistent finding. In conclusion, hypercapnia during acute loading primarily resulted from central-output inhibition of the diaphragm suggesting that acute loading responses are controlled by the cortex rather than bulbopontine centers.

New device for nonvolitional evaluation of quadriceps force in ventilated patients: Assessment of Quadriceps Force

In mechanically ventilated patients, nonvolitional assessment of quadriceps weakness using femoral‐nerve stimulation (twitch force) while the leg rests on a right‐angle trapezoid or dangles from the bed edge is impractical. Accordingly, we developed a knee‐support apparatus for use in ventilated patients.