Pearls and pitfalls of respiratory testing in a patient with amyotrophic lateral sclerosis and COPD.

Interpretation of pulmonary function testing in patients with amyotrophic lateral sclerosis must account for coexisting lung diseases, when making patient care decisions. https://bit.ly/3Co2yR0.

Inhibition of central activation of the diaphragm: a mechanism of weaning failure.

During a T-tube trial following disconnection of mechanical ventilation, patients failing the trial do not develop contractile diaphragmatic fatigue despite increases in inspiratory pressure output. Studies in volunteers, patients, and animals raise the possibility of spinal and supraspinal reflex mechanisms that inhibit central-neural output under loaded conditions. We hypothesized that diaphragmatic recruitment is submaximal at the end of a failed weaning trial despite concurrent respiratory distress. Tidal transdiaphragmatic pressure (ΔPdi) and electrical activity (ΔEAdi) were recorded with esophago-gastric catheters during a T-tube trial in 20 critically ill patients. During the T-tube trial, ∆EAdi was greater in weaning failure patients than in weaning success patients (P = 0.049). Despite increases in ΔPdi, from 18.1 ± 2.5 to 25.9 ± 3.7 cm H2O (P < 0.001), rate of transdiaphragmatic pressure development (from 22.6 ± 3.1 to 37.8 ± 6.7 cm H2O/s; P < 0.0004), and concurrent respiratory distress, ∆EAdi at the end of a failed T-tube trial was half of maximum, signifying inhibition of central neural output to the diaphragm. The increase in ΔPdi in the weaning failure group, while ∆EAdi remained constant, indicates unexpected improvement in diaphragmatic neuromuscular coupling (from 46.7 ± 6.5 to 57.8 ± 8.4 cm H2O/%; P = 0.006). Redistribution of neural output to the respiratory muscles characterized by a progressive increase in rib cage and accessory muscle contribution to tidal breathing and expiratory muscle recruitment contributed to enhanced coupling. In conclusion, diaphragmatic recruitment is submaximal at the end of a failed weaning trial despite concurrent respiratory distress. This finding signifies that reflex inhibition of central neural output to the diaphragm contributes to weaning failure.NEW & NOTEWORTHY Research into pathophysiology of failure to wean from mechanical ventilation has excluded several factors, including contractile fatigue, but the precise mechanism remains unknown. We recorded transdiaphragmatic pressure and diaphragmatic electrical activity in patients undergoing a T-tube trial. Diaphragmatic recruitment was submaximal at the end of a failed trial despite concurrent respiratory distress, signifying that inhibition of central neural output to the diaphragm is an important mechanism of weaning failure.

The effects of obesity on lung volumes and oxygenation.

INTRODUCTION: Obesity can cause hypoxemia by decreasing lung volumes to where there is closure of lung units during normal breathing. Studies describing this phenomenon are difficult to translate into clinical practice. We wanted to determine the lung volume measurements that are associated with hypoxemia in obese patients, and explore how we could use these measurements to identify them. METHODS: We collected pulmonary function test results and arterial blood gas data on 118 patients without obstruction on pulmonary function testing. We included only patients with normal chest imaging and cardiac testing within one year of the pulmonary function test, to exclude other causes of hypoxemia. RESULTS: We found that as BMI increases, the mean paO2, ERV % predicted, and ERV/TLC decrease (BMI 20-30 kg/m2: paO2=90±8 mmHg, ERV% predicted 112±50, ERV/TLC (%) 19.7±6.5; BMI 30-40 kg/m2: paO2=84±10 mmHg, ERV% predicted 84±40 ERV/TLC(%) 13.6±7.6; BMI>40 kg/m2: paO2 78 ±12 mmHg, ERV% predicted 64±27 ERV/TLC(%) 11.4±5.8, ANOVA p<0.001). The A-a gradient increases as BMI increases (r=0.42, p<0.001). This correlation was stronger in men (r=0.54) than in women (r=0.35). The paO2 is lower in patients with a low ERV than in those with a normal ERV (p<0.001). In a multivariate linear regression, only the ERV/TLC predicted (%), age, and BMI were associated with oxygenation (r2 for A-a gradient =0.28, p=0.036). CONCLUSIONS: In obese patients without cardiopulmonary disease, oxygen levels decrease as BMI increases. This effect is associated with the obesity-related reduction in ERV and is independent of hypoventilation.

Impact of obesity on respiratory function.

Obesity has long been recognized as having significant effects on respiratory function. The topic has been studied for at least the last half century, and some clear patterns have emerged. Obese patients tend to have higher respiratory rates and lower tidal volumes. Total respiratory system compliance is reduced for a variety of reasons, which will be discussed. Lung volumes tend to be decreased, especially expiratory reserve volume. Spirometry, gas exchange and airway resistance all tend to be relatively well preserved when adjusted for lung volumes. Patients may be mildly hypoxaemic, possibly due to ventilation-perfusion mismatching at the base of the lungs, where microatelectasis is likely to occur. Weight loss leads to a reversal of these changes. For all of these changes, the distribution of fat, that is, upper versus lower body, may be more important than body mass index.

Is the content of textbooks on the evaluation of a patient in respiratory distress adequate?

BACKGROUND: The ability to rapidly and precisely evaluate patients in respiratory distress is essential. Due to limited opportunities for formal instruction during training, textbooks are the main educational source to teach junior physicians how to interpret the signs of respiratory distress. The quality of the textbook content relevant to respiratory distress is unknown. OBJECTIVE: To examine the content on the evaluation of a patient in respiratory distress in a representative sample of textbooks and Internet resources. METHODS: Two physicians individually reviewed the most recent edition of 21 standard textbooks from a variety of specialties. Smartphone applications, UptoDate, and MD Consult were examined. Each physician reviewed the source for 14 different signs. For each sign, the reviewers determined 3 parameters: a mention of the sign, its pathophysiology, and its detection. The reviews were compared for discrepancies, and a third reviewer resolved them. RESULTS: The normal respiratory rate was mentioned in 10 (48%) of textbooks, and ranged between 10 and 22 breaths/min. Each sign was mentioned by a mean of 45 ± 26% of the textbooks. The pathophysiology of the signs was described by a mean of 33 ± 30% of the textbooks. The most and least commonly mentioned inspection signs were cyanosis and retraction of suprasternal notch, respectively. They were mentioned in 20 (95%) and 4 (19%) textbooks, respectively. The most and least commonly mentioned palpation signs were thoracoabdominal asynchrony or paradox and tracheal tug, respectively. They were mentioned in 17 (81%) and 4 (19%) textbooks, and their pathophysiology was described in 15 (71%) and 4 (19%) textbooks, respectively. The reviewers also found inconsistency in the descriptions of the meaning of scalene muscle contraction and thoracoabdominal asynchrony and paradox. CONCLUSIONS: The content of the reviewed textbooks on the evaluation of respiratory distress is inconsistent and deficient.

The pickwickian syndrome-obesity hypoventilation syndrome.

Obesity-hypoventilation syndrome (OHS), also historically described as the Pickwickian syndrome, consists of the triad of obesity, sleep disordered breathing, and chronic hypercapnia during wakefulness in the absence of other known causes of hypercapnia. Its exact prevalence is unknown, but it has been estimated that 10% to 20% of obese patients with obstructive sleep apnea have hypercapnia. OHS often remains undiagnosed until late in the course of the disease. Early recognition is important because these patients have significant morbidity and mortality. Effective treatment can lead to significant improvement in patient outcomes, underscoring the importance of early diagnosis. The authors review the definition and epidemiology of OHS, in addition to the current multifaceted understanding of the pathophysiology, and provide useful clinical approaches to diagnosis and treatment.