Three bedside techniques to quantify dynamic pulmonary hyperinflation in mechanically ventilated patients with chronic obstructive pulmonary disease

Background Dynamic pulmonary hyperinflation may develop in patients with chronic obstructive pulmonary disease (COPD) due to dynamic airway collapse and/or increased airway resistance, increasing the risk of volutrauma and hemodynamic compromise. The reference standard to quantify dynamic pulmonary hyperinflation is the measurement of the volume at end-inspiration (Vei). As this is cumbersome, the aim of this study was to evaluate if methods that are easier to perform at the bedside can accurately reflect Vei. Methods Vei was assessed in COPD patients under controlled protective mechanical ventilation (7 ± mL/kg) on zero end-expiratory pressure, using three techniques in a fixed order: (1) reference standard (Veireference): passive exhalation to atmosphere from end-inspiration in a calibrated glass burette; (2) ventilator maneuver (Veimaneuver): measuring the expired volume during a passive exhalation of 45s using the ventilator flow sensor; (3) formula (Veiformula): (Vt × Pplateau)/(Pplateau − PEEPi), with Vt tidal volume, Pplateau is plateau pressure after an end-inspiratory occlusion, and PEEPi is intrinsic positive end-expiratory pressure after an end-expiratory occlusion. A convenience sample of 17 patients was recruited. Results Veireference was 1030 ± 380 mL and had no significant correlation with Pplateau (r2 = 0.06; P = 0.3710) or PEEPi (r2 = 0.11; P = 0.2156), and was inversely related with Pdrive (calculated as Pplateau −PEEPi) (r2 = 0.49; P = 0.0024). A low bias but rather wide limits of agreement and fairly good correlations were found when comparing Veimaneuver and Veiformula to Veireference. Vei remained stable during the study period (low bias 15 mL with high agreement (95% limits of agreement from − 100 to 130 mL) and high correlation (r2 = 0.98; P < 0.0001) between both measurements of Veireference). Conclusions In patients with COPD, airway pressures are not a valid representation of Vei. The three techniques to quantify Vei show low bias, but wide limits of agreement.

Tracheal Adenocarcinoma in a Cat

Background: Primary tracheal adenocarcinoma is a rare neoplasm in cats. The clinical signs often are indicative of upper airway obstruction accompanied with dyspnea, stridor, wheezing, exercise intolerance, and cough. The severity of the clinical signs is related to the size of the mass and consequently, the proportion of the tracheal lumen that is obstructed. The diagnosis is made using thoracic radiography and tracheobronchoscopy by collecting fragments for histopathological analysis and removing the mass. The present study aimed to report the case of a cat with tracheal adenocarcinoma.Case: A 17-year-old Persian female cat presented with clinical signs of dyspnea and progressive weight loss. Emergency therapy was started with bronchodilators, antibiotics, and corticosteroids, but there was no response to treatment. Complementary blood and imaging tests were performed. Thoracic radiography revealed soft tissue opacity overlying the dorsal trachea from the third to the fourth rib, bronchial pattern, and pulmonary hyperinflation. Tracheoscopy showed an irregular intraluminal thoracic trachea mass, occluded by approximately 95% of the airway lumen. The mass was biopsied multiple times with endoscopic cup biopsy forceps, followed by removal of approximately 50% of the mass lesion with an endoscopic wire snare. The patient was in intensive care, and since her clinical condition worsened 48 h after the endoscopic procedure, euthanasia was performed. Necropsy revealed a remanescent mass located in the trachea lumen 8 x 3 mm and a nodule in the right caudal pulmonary lobe with 8 mm of diameter . Histological examination showed epitelian cuboidal neoplastic cells with acinar patterns. Only a few mitosis and moderate anysocitosis were observed. The final diagnosis was primary tracheal adenocarcinoma with pulmonary metastasis.Discussion: The initial oxygen therapy associated with bronchodilators and antibiotics can be explained by the history of asthma. Tracheal tumors in cats are considered to be rare, which makes the diagnosis challenging. The suspicion of tracheal neoplasia was only raised after radiographic examination, but it was not possible to state whether it was intra- or extratracheal. The bronchial pattern reported herein can be observed both in inflammatory diseases such as asthma and bronchitis as well as aging-related diseases in animals. Pulmonary hyperinflation, with a caudal displacement of the diaphragm, is seen in bronchial diseases and in cases of tracheal neoplasms, with the latter justified by the retention of air in the pulmonary lobes. Dehydration and weight loss in the animal are justified by severe dyspnea, which makes it difficult to consume food and water. The tracheoscopy procedure was essential to confirm intraluminal tracheal neoplasia with almost complete lumen obstruction. An attempt was made to remove the neoplasms with polypectomy endoscopic forceps. However, because 95% of the trachea was obstructed, the manipulation led to local edema and bleeding, which promoted complete obstruction of the air passage to the lungs. The obstruction impaired the patient's oxygenation, justifying procedure suspension. The instability and worsening of the clinical picture persisted in the subsequent days, which prevented further intervention, culminating in the animal's euthanasia. Adenocarcinoma, in the present case, was in the advanced stage, evidenced by the presence of pulmonary metastasis. Dyspnea severity was related to neoplasm size, proportion of tracheal lumen obstruction, and presence of pulmonary metastasis. The tumor size associated with the presence of metastasis was a determining factor for the classification of neoplasia in the advanced stage, making more invasive interventions impossible and worsening the patient prognosis.

RECENT ASPECTS OF CARDIAC REMODELING IN PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE

The paper aimed to present evidence of the effect of some pathophysiological features of chronic obstructive pulmonary disease (COPD) on cardiac remodeling in patients free of overt cardiovascular diseases, traditional cardiovascular risk factors and pulmonary hypertension. Contrary to traditional beliefs that cardiac abnormalities in COPD have been mainly associated with the right ventricle, several recent studies have shown an independent effect of pulmonary hyperinflation and emphysema on left ventricular (LV) diastolic filling and LV hypertrophy. Pulmonary hyperinflation and emphysema cause intrathoracic hypovolemia, low preload, small end-diastolic dimension and mechanical compression of LV chamber which could worsen end-diastolic stiffness. Interestingly, that the presence of LV hypertrophy in COPD patients is important but currently poorly understood area of investigation. Pulmonary hyperinflation, increased arterial stiffness and sympathetic activation may be associated with LV hypertrophy. Two-dimensional ultrasound speckle tracking studies have shown the presence of sub-clinical LV systolic dysfunction in patients even with moderate COPD and free of overt cardiovascular diseases. Sarcopenia related to the inflammatory-catabolic state in COPD and hypoxia could play an important role regarding LV systolic dysfunction. Recent data reported the effects of long-acting bronchodilators on reducing lung hyperinflation (inducing lung deflation). Further studies are required to evaluate the effects of pharmacological lung deflation therapy on cardiac volume and function.