Negative Intrathoracic Pressure Research Articles

NEGATIVE PRESSURE PULMONARY EDEMA FOLLOWING RELIEF OF UPPER AIRWAY OBSTRUCTION

SESSION TITLE: Wednesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Obstructive sleep apnea (OSA) is associated with fragmented sleep caused by intermittent narrowing or occlusion of the upper airways leading to hypoxia. Uvulopalatopharyngoplasty (UPPP) is a common surgical treatment for adult patients with OSA. Complications are infrequent post-UPPP and include respiratory failure, hemorrhage, and hypertension. We report a serious complication of negative pressure pulmonary edema (NPPE) leading to respiratory failure after a UPPP procedure. CASE PRESENTATION: A 33 year-old-male with a past medical history of morbid obesity and OSA underwent UPPP without intraoperative complications. Immediately following extubation, he developed hypoxia refractory to increasing oxygen supplementation requiring intubation. The post intubation chest X-ray (CXR) showed diffuse pulmonary edema with a deep sulcus sign on the right. Extensive pink frothy secretions were suctioned repeatedly and required an endotracheal tube exchange. The repeat CXR showed worsening pulmonary edema and a right-sided pneumothorax which failed to improve despite right-sided chest tube placement. He subsequently required a second right-sided chest tube which expanded the right lung, decreased the peak pressures, and improved oxygenation. Echocardiogram was consistent with longstanding OSA and revealed a moderate to severely dilated right ventricle with reduced function. Patient’s condition improved rapidly with diuretics and aggressive mechanical ventilation; he was weaned off the ventilator and the chest tubes were quickly removed. After a short hospital course, he was discharged home in stable condition. DISCUSSION: The temporal cause of events following the relief of upper airway obstruction after UPPP suggests that NPPE was the cause of the respiratory failure. Clinicians need to be aware of this serious complication as rapid recognition can improve outcomes. NPPE can be classified as either Type I or Type II. Type I develops in patients who generate a negative intrathoracic pressure against acute airway obstruction. This can occur in patients with upper airway infections and laryngospasms leading to increased venous return and pulmonary edema. Type II develops after relief of chronic upper airway obstruction with loss of positive end-expiratory pressure (PEEP). The rapid removal of PEEP leads to interstitial fluid transudation and pulmonary edema. Regardless of type, patients usually present with hypoxia, pulmonary edema, and pink frothy sputum. Manifestations of acute airway obstruction may be present and include stridor with use of accessory muscles. Management is supportive with or without the use of diuretics. The use of positive airway pressure ventilation has been suggested for both acute management and prevention of pulmonary edema. CONCLUSIONS: Although a benign surgical procedure, UPPP has complications that need to be rapidly identified in the immediate post-operative period. Reference #1: Bhaskar B, Fraser JF. Negative pressure pulmonary edema revisited: Pathophysiology and review of management. Saudi J Anaesth. 2011;5(3):308-13. Reference #2: Miro AM, Shivaram U, Finch PJ. Noncardiogenic pulmonary edema following laser therapy of a tracheal neoplasm. Chest. 1989;96:1430–1. Reference #3: Guffin TN, Harel G, Sanders A, Lucente FE, Nash M. Acute postobstructive pulmonary edema. Otolaryngol Head Neck Surg. 1995;112:235–7. DISCLOSURES: No relevant relationships by Abdullah Al Twal, source=Web Response No relevant relationships by Kristin Fless, source=Web Response No relevant relationships by Sasa Ivanovic, source=Web Response No relevant relationships by Nirav Mistry, source=Web Response No relevant relationships by Vagram Ovnanian, source=Web Response No relevant relationships by Anish Patel, source=Web Response No relevant relationships by Fariborz Rezai, source=Web Response No relevant relationships by Paul Yodice, source=Web Response

Idiopathic pulmonary fibrosis and GERD: links and risks.

Gastroesophageal reflux disease (GERD) and idiopathic pulmonary fibrosis (IPF) are two pathological conditions often strictly related, even if a clear relationship of causality has not been demonstrated. GERD is a frequent comorbidity in IPF patients, as demonstrated using combined multichannel intraluminal impedance-pH, despite being mostly clinically silent. According to that, it has been hypothesized that microaspiration of gastric material may play a fundamental role in the fibrotic transformation of pulmonary parenchyma. In contrast, it cannot be excluded that IPF may favor GERD by increasing the negative intrathoracic pressure. Therefore, this relationship is uncertain as well as not univocal. Nevertheless, the latest international guidelines recommend the use of proton pump inhibitors (PPIs) in IPF based on several data showing that PPIs can stabilize lung function, reduce disease flares and hospitalizations. On the contrary, recent studies not only question the relevance of these results, but also associate the use of PPIs with an increased risk of lung infections and a negative prognostic outcome. The aim of this review is to analyze the possible links between GERD and IPF and their possible therapeutic implications, trying to translate this scientific evidence into useful information for clinical practice.

Current understanding of the effects of inspiratory resistance on the interactions between systemic blood pressure, cerebral perfusion, intracranial pressure, and cerebrospinal fluid dynamics.

Negative intrathoracic pressure (nITP) is generated by the respiratory muscles during inspiration to overcome inspiratory resistance, thus enabling lung ventilation. Recently developed noninvasive techniques have made it possible to assess the effects of nITP in real time in several physiological aspects such as systemic blood pressure (BP), intracranial pressure (ICP), and cerebral blood flow (CBF). It has been shown that nITP from 0 to -20 cmH2O elevates BP and diminishes ICP, which facilitates brain perfusion. The effects of nITP from -20 to -40 cmH2O on BP, ICP, and CBF remain largely unrecognized, yet even nITP at -40 cmH2O may facilitate CBF by diminishing ICP. Importantly, nITP from -20 to -40 cmH2O has been documented in adults in commonly encountered obstructive sleep apnea, which justifies research in this area. Recent revelations about interactions between ICP and BP have opened up new fields of research in physiological regulation and the pathophysiology of common diseases, such as hypertension, brain injury, and respiratory disorders. A better understanding of these interactions may translate directly into new therapies in various fields of clinical medicine.

Prolonged respiratory failure due to pulmonary embolism in a young woman: a case report

BackgroundThe pathophysiology of pulmonary edema is generally considered to result from elevated pulmonary capillary hydrostatic pressure due to increased left atrial pressure in consequence of a failing left ventricle.Case presentationWe present a case of pulmonary edema secondary to severe hypalbuminemia under excessive respiratory drive in a 29-year-old Caucasian woman in respiratory distress with detected bilateral central pulmonary embolism.ConclusionIn conjunction with severe hypalbuminemia, even the negative intrathoracic pressure swings of respiratory distress may cause pulmonary edema. Detrimental consequences of non-invasive ventilation due to uncontrolled tidal volume and pressure swings need to be considered when treating patients in hypoxemic respiratory failure with low serum albumin.

Impaired central hemodynamics in chronic obstructive pulmonary disease during submaximal exercise.

It is unknown whether central hemodynamics are impaired during exercise in chronic obstructive pulmonary disease (COPD) patients. We hypothesized that, at a similar absolute V̇o2 during exercise, COPD patients would have a lower stroke volume and cardiac output compared with healthy controls. Furthermore, we hypothesized that greater static hyperinflation [ratio of inspiratory capacity to total lung capacity (IC/TLC)] and expiratory intrathoracic pressure would be significantly related to the lower cardiac output and stroke volume responses in COPD patients. Clinically stable COPD (n = 13; FEV1/FVC: 52 ± 13%) and controls (n = 10) performed constant workload submaximal exercise at an absolute V̇o2 of ~1.3 L/min. During exercise, inspiratory capacity maneuvers were performed to determine operating lung volumes and cardiac output (via open-circuit acetylene rebreathe technique) and esophageal pressure were measured. At similar absolute V̇o2 during exercise (P = 0.81), COPD had lower cardiac output than controls (COPD: 11.0 ± 1.6 vs. control: 12.2 ± 1.2 L/min, P = 0.03) due to a lower stroke volume (COPD: 107 ± 13 vs. control: 119 ± 19 mL, P = 0.04). The heart rate response during exercise was not different between groups (P = 0.66). FEV1 (%predicted) and IC/TLC were positively related to stroke volume (r = 0.68, P = 0.01 and r = 0.77, P < 0.01). Last, esophageal pressure-time integral during inspiration was positively related to cardiac output (r = 0.56, P = 0.047). These data demonstrate that COPD patients have attenuated cardiac output and stroke volume responses during exercise compared with control. Furthermore, these data suggest that the COPD patients with the most severe hyperinflation and more negative inspiratory intrathoracic pressures have the most impaired central hemodynamic responses.NEW & NOTEWORTHY Chronic obstructive pulmonary disease leads to cardiac structural changes and pulmonary derangements that impact the integrative response to exercise. However, it is unknown whether these pathophysiological alterations influence the cardiac response during exercise. Herein, we demonstrate that COPD patients exhibit impaired central hemodynamics during exercise that are worsened with greater hyperinflation.

Mechanisms of inspiration that modulate cardiovascular control: the other side of breathing.

The objective of this minireview is to describe the physiology and potential clinical benefits derived from inspiration. Recent animal and clinical studies demonstrate that one of the body's natural mechanisms associated with inspiration is to harness the respiratory pump to enhance circulation to vital organs. There is evidence that large reductions in intrathoracic pressure (>20 cmH2O) caused by some inspiration maneuvers (e.g., Mueller maneuver) or pathophysiology (e.g., heart failure, chronic obstructive lung disease) can result in adverse hemodynamic effects. However, the respiratory pump can improve cardiovascular functions when a "sweet spot" for generation of negative intrathoracic pressure during inspiration can be maintained at or less than 10 cmH2O below normal inspiration. These beneficial physiological effects include greater cardiac filling and output, lower intracranial pressure, cardiac baroreflex resetting, greater cerebral blood flow oscillatory patterns, increased vascular pressure gradients, and promoting sustained feedback between sympathetic nerve activity and arterial pressure. In addition to promoting gas exchange, data obtained from numerous animal and human experiments have provided new insights into "the other side of breathing": the modulation of circulation by reduced intrathoracic pressure generated during inspiration. The translation of these physiological relationships form the basis for the development and application of technologies designed to optimize the intrathoracic pump for treatment of clinical conditions associated with hypovolemia including cardiac arrest, orthostatic hypotension, hemorrhagic shock, and traumatic brain injury. Harnessing these fundamental mechanisms that control cardiopulmonary physiology provides opportunities to use inspiration as a potential tool to help treat significant and often life-threatening circulatory disorders.

Effects of Optimizing the Respiratory Pump on Performance During a Simulated Ice Hockey Period

Ice hockey requires high-intensity activity during shifts with inactive recovery between shifts. During recovery periods, blood may pool in the legs, reducing central blood volume and the ability to clear lactic acid. Impedance threshold devices (ITD) were developed to treat conditions of central hypovolemia, such as hemorrhage. By creating a negative intrathoracic pressure, venous return is enhanced, increasing stroke volume and cardiac output. PURPOSE: To determine the effects of breathing with an ITD during recovery periods between simulated ice hockey shifts. METHODS: Five male collegiate ice hockey players skated a course, the Peterson On-Ice Repeated Sprint Test, eight times (shifts) with 90 s recovery between each shift. Each athlete completed two test sessions separated by 48 hr, one while breathing freely during the recovery periods (control condition) and one while breathing with the ITD during the recovery periods. RESULTS: Performance, measured as time to skate the course, was similar between conditions (p > .05). Average time to complete each shift was 22.10 ± 0.74 s (SEM) and increased with successive shifts. After shift 4, lactate was 12.0 ± 0.8 mM (control) and 11.0 ± 2.0 mM (ITD). After skating eight shifts, lactate continued to increase during the control condition (14.0 ± 0.4 mM) and was 28% higher than the ITD condition (10.9 ± 1.5 mM). Ratings of perceived exertion increased from shift 1 to shift 8 with the average slope of increase greater for the control condition (0.87, 95% CI 0.80-0.94) than the ITD condition (0.65, 95% CI 0.60-0.70, Z = -7.54, p < .001). CONCLUSIONS: Breathing with the ITD during recovery periods did not affect skating performance measured as time to complete each shift, but lactate was lower after shift 8 and athletes rated their exertion lower during the ITD condition. Thus, use of an ITD has potential to enhance recovery during repeated bouts of high-intensity, intermittent exercise.

Sleep Disordered Breathing and Cardiovascular Diseases.

Sleep disordered breathing (SDB), which causes sleep deprivation, intermittent hypoxia, and negative intrathoracic pressure swings, can be accompanied by other harmful pathophysiologies relating to cardiovascular diseases (CVD), including sudden death, atrial fibrillation, stroke, and coronary artery disease leading to heart failure. Continuous positive airway pressure (CPAP) therapy for SDB has been reported to provide favorable effects such as lowered systemic blood pressure and improved endothelial function. However, in recent randomized controlled trials, CPAP has failed to demonstrate its beneficial prognostic impact on the primary or secondary setting of CVD. In this review article, we describe the characteristics of SDB complicated with CVD, the prognostic impacts of SDB in CVD, and the beneficial effects of CPAP on CVD.

Vascular responses to hypoxia are not impaired in obstructive sleep apnoea patients free of overt cardiovascular disease.

What is the central question of this study? Does treatment of obstructive sleep apnoea (OSA) with nocturnal oxygen or continuous positive airway pressure (CPAP) improve hypoxic vascular responses, which are reportedly impaired in OSA? What is the main finding and its importance? Cerebrovascular and cardiovascular hypoxic responses were not impaired in OSA patients free of overt cardiovascular disease and known risk factors, and were not altered by nocturnal oxygen or CPAP treatment. We conclude that this OSA patient phenotype has normal vascular responses to hypoxia and is unlikely to obtain long term cardiovascular benefits from nocturnal oxygen or CPAP therapy. Cerebral blood flow (CBF) and cardiovascular responses to hypoxia are reportedly impaired in obstructive sleep apnoea (OSA) patients and corrected by continuous positive airway pressure (CPAP), beneficial effects that are ascribed to correction of OSA-related intermittent hypoxia (IH). However, CPAP corrects both IH and ancillary OSA features (i.e. intermittent hypercapnia, sympathetic activation, blood pressure surges, negative intrathoracic pressure swings and sleep fragmentation). Whether correction of these ancillary OSA features contribute to CPAP's beneficial effects on vascular hypoxic responses is unknown. Nocturnal oxygen corrects OSA-induced IH, but apnoeas and ancillary features persist. Thus, we examined the effects of nocturnal oxygen and CPAP on cerebrovascular and cardiovascular hypoxic responses in untreated OSA patients. Responses were assessed in 52 OSA patients free of overt cardiovascular disease and known risk factors at baseline, after 2weeks of nocturnal oxygen (n=26) or no treatment (n=26), and after ∼4weeks of CPAP treatment (n=40). Twenty-two age-matched controls were assessed at baseline and follow-up visits. Resting, isocapnic euoxia mean blood pressure was decreased following nocturnal oxygen (-3.6±6.0mmHg; P=0.006) and CPAP (-4.5±7.5mmHg; P<0.001) while cerebrovascular conductance was increased with CPAP (P=0.001). However, these changes were not different from controls. Unexpectedly, OSA patients and controls had similar hypoxic vascular responses at baseline that were not changed by either nocturnal oxygen or CPAP. We conclude that OSA patients free of overt cardiovascular disease and known risk factors did not have impaired cerebrovascular or cardiovascular responses to hypoxia and are unlikely to obtain long term cardiovascular benefits from nocturnal oxygen or CPAP therapy.

Clinical characteristic and management of descending necrotizing mediastinitis: a retrospective study, Dr. Soetomo Hospital, Surabaya

Background: Descending necrotizingmediastinitis (DNM) is a mediastinal infection that is usually an extensionor process of spreading an infection originating from the neck. The spread ofinfection occurs due to the influence of gravity and negative intrathoracicpressure. Methods: We collect data from medical record patients whopresented with DNM at Dr. Soetomo General Hospital , Surabaya, Indonesia,from January 2013 to December 2017. We collect characteristic data of eachpatient, diagnostic, operative management and outcome. Results: We have 56 patients met inclusion criteria, Therewere 50 patients came to our hospital with preoperative septicemia. The sourceof infection that we found, odontogenic 30 cases (53.57%), we did cervicotomysubsternal drainage for 54 cases (96.43%), sternotomy 1 (1.79%) and rightthoracotomy 1 (1.79%). Our mortality is 14.29%/5 years. Conclusions: Transcervical mediastinal drainageand adequate debridement is effective. Transthoracic mediastinal drainage wasdepended on each case. Thoracotomy if locus infection or pus accumulation onpleura. Sternotomy approach if locus infection is wide spreading tomediastinum, right or left pleura.

Cardiac rhythm disorders in obstructive sleep apnea.

Obstructive sleep apnea (OSA) is common among patients with cardiac rhythm disorders. OSA may contribute to arrhythmias due to acute mechanisms, such as generation of negative intrathoracic pressure during futile efforts to breath, intermittent hypoxia, and surges in sympathetic activity. In addition, OSA may lead to heart remodeling and increases arrhythmia susceptibility. Atrial distension and remodeling, that has been shown to be associated with OSA, is a well-known anatomical substrate for atrial fibrillation (AF). AF is the arrhythmia most commonly described in patients with OSA. Several observational studies have shown that the treatment of OSA with continuous positive airway pressure (CPAP) reduces recurrence of AF after electrical cardioversion and catheter ablation. There is also evidence that nocturnal hypoxemia, a hallmark of OSA, predicts sudden cardiac death (SCD) independently of well-established cardiovascular risk factors. Among patients with an implantable cardiac defibrillator, those with OSA have a higher risk of receiving treatment for life-threatening arrhythmias. Nocturnal hypoxemia may also increase vagal tone, which increases susceptibility to bradycardic and conduction rhythm disorders that have also been described in patients with OSA. In conclusion, there are several biological pathways linking OSA and increased cardiac arrhythmogenesis propensity. However, the independent association is derived from observational studies and the direction of the association still needs clarification due to the lack of large clinical trials. This review focuses on the current scientific evidence linking OSA to cardiac rhythm disorders and point out future directions.

Mechanisms and Major Sites of Distal Catheter Migration in Ventriculoperitoneal Shunting Maneuvers: A Review Article

A ventriculoperitoneal shunt (VPS) is a medical device used to deflect cerebrospinal fluid from cerebral ventricles to the peritoneal cavity. Since 1908, ventriculoperitoneal shunts have been considered the best option in hydrocephalus management. Manifestation related to VPS may arise anywhere whilst tunneling the VPS from the ventricle to the peritoneal cavity, but complications associated with the distal catheter are especially common and a leading cause of revision surgeries. Among the many complications associated with peritoneal shunts, migration of the catheter into other parts of the body is still common. Scrotal migration mainly takes place in children aged 4 days to 5 years. Patent processus vaginalis, formation of an inguinal hernia, and increased intraabdominal pressure are leading risk factors associated with migration of the peritoneal catheter into the scrotum. Thoracic migration of peritoneal catheters predominantly occurs in adult patients. Important mechanisms in thoracic migration include (1) iatrogenic perforation of the external or internal jugular veins by the surgeon during tunneling and (2) gradual destruction of the venous structures by the catheter due to routine extension and flexion of the neck. After entering the vessel, negative intrathoracic pressure combined with positive intraabdominal pressure aids migration into the thoracic cavity. Sharp tips or shunt types contribute to intraabdominal migration and perforation.

Exosome and Macrophage Crosstalk in Sleep-Disordered Breathing-Induced Metabolic Dysfunction.

Obstructive sleep apnea (OSA) is a highly prevalent worldwide public health problem that is characterized by repetitive upper airway collapse leading to intermittent hypoxia, pronounced negative intrathoracic pressures, and recurrent arousals resulting in sleep fragmentation. Obesity is a major risk factor of OSA and both of these two closely intertwined conditions result in increased sympathetic activity, oxidative stress, and chronic low-grade inflammation, which ultimately contribute, among other morbidities, to metabolic dysfunction, as reflected by visceral white adipose tissue (VWAT) insulin resistance (IR). Circulating extracellular vesicles (EVs), including exosomes, are released by most cell types and their cargos vary greatly and reflect underlying changes in cellular homeostasis. Thus, exosomes can provide insights into how cells and systems cope with physiological perturbations by virtue of the identity and abundance of miRNAs, mRNAs, proteins, and lipids that are packaged in the EVs cargo, and are secreted from the cells into bodily fluids under normal as well as diseased states. Accordingly, exosomes represent a novel pathway via which a cohort of biomolecules can travel long distances and result in the modulation of gene expression in selected and targeted recipient cells. For example, exosomes secreted from macrophages play a critical role in innate immunity and also initiate the adaptive immune response within specific metabolic tissues such as VWAT. Under normal conditions, phagocyte-derived exosomes represent a large portion of circulating EVs in blood, and carry a protective signature against IR that is altered when secreting cells are exposed to altered physiological conditions such as those elicited by OSA, leading to emergence of IR within VWAT compartment. Consequently, increased understanding of exosome biogenesis and biology should lead to development of new diagnostic biomarker assays and personalized therapeutic approaches. Here, the evidence on the major biological functions of macrophages and exosomes as pathophysiological effectors of OSA-induced metabolic dysfunction is discussed.

Obstructive sleep apnea in patients with chronic thromboembolic pulmonary hypertension.

Due to its effects, like an exaggerated negative intrathoracic pressure, sympathetic activation, systemic inflammation, oxidative stress, and endothelial dysfunction, obstructive sleep apnea (OSA) has been involved as a cause in multiple cardiovascular diseases. These diseases include coronary artery disease, hypertension, heart failure, and pulmonary hypertension (PH). Furthermore, OSA often coexists with chronic thromboembolic pulmonary hypertension (CTEPH) in clinical practice. However, few studies focus on OSA and its relationship with CTEPH. This study aims to determine whether OSA has an influence on the clinic status of patients with CTEPH, and to identify what possible factors are associated with OSA in CTEPH. Patients who were newly diagnosed with CTEPH and received overnight polysomnography (PSG) monitoring from September 2015 to December 2017 were enrolled. OSA was defined as apnea-hypopnea index (AHI) of ≥5/h and the obstructive events at ≥50%. Baseline clinical characteristics and parameters were collected and compared between CTEPH patients with and without OSA. In addition, logistic regression analysis was performed to identify possible factors associated with OSA in CTEPH. Fifty-seven patients with CTEPH were eventually enrolled. Among them, 32 patients were diagnosed with OSA by PSG. CTEPH patients with OSA showed an older age, a higher body mass index (BMI), a higher hemoglobin level, a lower oxygen saturation and a worse World Health Organization functional class (WHO FC) (all P<0.05) when compared to CTEPH patients without OSA. In addition, sleep data including AHI, oxygen desaturation index and minimum oxygen saturation were also statistically different between two groups (all P<0.05). Adjusted for age, sex and BMI, hemoglobin [odd ratio (OR) =1.057, 95% confidence interval (CI): 1.001-1.117, P=0.046], oxygen saturation (OR =0.718, 95% CI: 0.554-0.929, P=0.012), N-terminal pro-brain natriuretic peptide (OR =1.001, 95% CI: 1.000-1.002, P=0.016), mean right atrium pressure (OR =1.284, 95% CI: 1.030-1.600, P=0.026), mean pulmonary arterial pressure (mPAP) (OR =1.087, 95% CI: 1.001-1.180, P=0.048), cardiac index (CI) (OR =0.058, 95% CI: 0.008-0.433, P=0.037), pulmonary vascular resistance (OR =1.004, 95% CI: 1.001-1.007, P=0.014) and WHO FC III-IV (OR =18.550, 95% CI: 2.363-144.128, P=0.005) were associated with OSA in CTEPH. Multivariate logistic regression analysis demonstrated CI (OR =0.051, 95% CI: 0.003-0.868, P=0.040) was independently associated with OSA in CTEPH in addition to age, sex and BMI. OSA may aggravate the clinical status of CTEPH patients to some degree. In turn, a worse hemodynamics, oxygenation state and cardiac function are associated with OSA in CTEPH after being adjusted for age, sex and BMI. Among them, CI is the most important parameter in indicating the coexistence of OSA and CTEPH.

Clarifying the link between sleep disordered breathing and tracheal collapse: a retrospective analysis

BackgroundSymptoms of acquired tracheobronchomalacia (TBM) include wheezing, shortness of breath, and chronic cough, and can negatively affect quality of life. Successful treatment of TBM requires identification of the disorder and of contributing factors. Acquired TBM is generally associated with a number of conditions, including asthma, chronic obstructive pulmonary disease (COPD), and gastroesophageal reflux. Although a possible relationship with obstructive sleep apnea (OSA) has been observed, data illuminating such an interaction are sparse.MethodsIn the present study, we analyzed the percent tracheal collapse (as measured on dynamic chest CT) and detailed sleep reports of 200 patients that had been seen at National Jewish Health, half of which had been diagnosed with OSA and half which did not have OSA.ResultsTracheal collapse ranged from 0 to 99% closure in the population examined, with most subjects experiencing at least 75% collapse. OSA did not relate significantly to the presence or severity of tracheobronchomalacia in this population. Sleep disordered breathing (SDB) did show a strong association with TBM (p < 0.03).ConclusionsTracheobronchomalacia may develop as a result of increased negative intrathoracic pressure created during attempts at inhalation against a closed or partially closed supraglottic area in patients experiencing apneic or hypopneic events, which contributes to excessive dilation of the trachea. Over time, increased airway compliance develops, manifesting as tracheal collapse during exhalation. Examining TBM in the context of SDB may provide a reasonable point at which to begin treatment, especially as treatment of sleep apnea and SDB (surgical or continuous positive airway pressure) has been shown to improve associated TBM.

Sex differences in diaphragmatic fatigue and the metaboreflex following inspiratory pressure-threshold loading.

Sex differences in diaphragmatic fatigue and the metaboreflex following inspiratory pressure-threshold loading.

New insights into the timing and potential mechanisms of respiratory-induced cortical arousals in obstructive sleep apnea

A negative intrathoracic pressure threshold is one commonly proposed mechanism for triggering respiratory-induced arousals in obstructive sleep apnea (OSA). If so, they should occur during inspiration, shortly after maximal negative pressure swings. Alternatively, respiratory-induced arousals may occur throughout the respiratory cycle if other mechanisms also contribute. However, arousal timing has been minimally investigated. This study aimed to (1) determine the temporal relationship between respiratory-induced arousals and breathing phase and (2) characterize neuromuscular and load compensation responses prior to arousal. Fifty-one CPAP-treated OSA patients underwent a sleep physiology study with genioglossus and tensor palatini EMG, nasal mask/pneumotachograph, and epiglottic pressure. Transient CPAP reductions were delivered to induce respiratory-related arousals. Of 354 arousals, 65(60-70)%[mean(CI)] occurred during inspiration, 35(30-40)% during expiration. Nadir epiglottic pressure occurred 68(66-69)% into inspiration while inspiratory arousals had a uniform distribution throughout inspiration. Expiratory arousals occurred predominantly in early expiration. CPAP reductions initially reduced minute ventilation by ~2.5 liter/min, which was restored immediately prior to expiratory but not inspiratory arousals. Duty cycle just prior to arousal was greater for inspiratory versus expiratory arousals [0.20(0.18-0.21) vs. 0.13(0.11-0.15)Δbaseline, p = 0.001]. Peak tensor palatini EMG was higher for expiratory versus inspiratory arousals during prearousal breaths [7.6(5.8-9.6) vs. 3.7(3.0-4.5)%Δbaseline, p = 0.001], whereas genioglossus and tonic tensor palatini EMG were similar between arousal types. Over one third of respiratory-induced arousals occur during expiration. These findings highlight the importance of nonpressure threshold mechanisms of respiratory-induced arousals in OSA and suggest that expiratory arousals may be a novel marker of enhanced tensor palatini neuromuscular compensation.

¿El reflujo gastroesofágico y la aspiración de contenido gástrico están implicados en la etiopatogenia y la progresión de la fibrosis pulmonar idiopática?

ABSTRACT Gastroesophageal reflux (GERD) and hidden aspiration of gastric contents are probably involved in the pathogenesis and progression of idiopathic pulmonary fibrosis (IPF). The pathological mechanisms involved are decreased pulmonary distensibility and consequent increase of intrathoracic negative pressure during inspiration, as well as decreased control mechanisms of esophageal motility or lower esophageal sphincter. The prevalence of GERD and oesophageal dysmotility was higher in patients with IPF as compared with general population. Among patients with IPF, 67-76% demonstrated abnormal oesophageal acid exposure. However, no relationship was demonstrated between severity of GERD and severity of IPF. Data are scant on outcomes of antireflux treatment in patients with IPF. Actually, some data suggests that antacid treatment may be deleterious in some IPF patients. After analyzing all the relevant evidence found to date, a causal relationship between GERD, gastric content aspiration and IPF pathogenesis cannot be established. There is scant evidence examining antireflux treatment in idiopathic pulmonary fibrosis patients.

Sternotomy and ventral slot decompression for treatment of T1-2 intervertebral disk disease in a Dachshund

CASE DESCRIPTION A 9-year-old 7.5-kg (16.5-lb) castrated male Dachshund was referred for emergency evaluation of pelvic limb paraplegia of < 24 hours' duration. CLINICAL FINDINGS A spinal cord lesion between T3 and L3 was suspected given the dog's history and neurologic examination results. Computed tomography and myelography spanning T3 through L4 identified an extradural compressive lesion at the L3-4 disk space. Hemilaminectomy was performed, and disk material adhered to and compressing the spinal cord was identified. However, because the material appeared to have been present for an extended period, postoperative CT of the cervicothoracic region was performed, which revealed extrusion of disk material from the T1-2 space and marked spinal cord compression. TREATMENT AND OUTCOME A sternotomy of the manubrium and ventral slot decompression of the T1-2 disk space were performed successfully without entering the thoracic cavity. A large amount of disk material was removed from the spinal canal. No loss of intrathoracic negative pressure was appreciated, and intraoperative complications included only mild hemorrhage. The dog maintained pelvic limb pain sensation postoperatively and regained motor function 2 days after surgery. CLINICAL RELEVANCE Intervertebral disk disease is rare at T1-2 in Dachshunds. Typically, a dorsal approach has been used to decompress the spinal cord, but findings for this dog suggested that a ventral approach may also be appropriate. Consideration should be given to include the T1-2 disk space when performing advanced imaging in dogs because of the inconsistent ability to identify lesions at this location by means of neurologic examination.

P38 Inhibition Ameliorates Inspiratory Resistive Breathing-Induced Pulmonary Inflammation.

Inspiratory resistive breathing (IRB), a hallmark of obstructive airway diseases, is associated with strenuous contractions of the inspiratory muscles and increased negative intrathoracic pressures that act as an injurious stimulus to the lung. We have shown that IRB induces pulmonary inflammation in healthy animals. p38 kinase is activated in the lung under stress. We hypothesized that p38 is activated during IRB and contributes to IRB-induced pulmonary inflammation. Anesthetized, tracheostomized rats breathed spontaneously through a two-way valve. Resistance was connected to the inspiratory port to provoke a peak tidal inspiratory pressure 50% of maximum. Following 3 and 6h of IRB, respiratory system mechanics were measured and bronchoalveolar lavage (BAL) was performed. Phosphorylated p38, TNF-α, and MIP-2α were detected in lung tissue. Lung injury was estimated histologically. SB203580 (p38 inhibitor) was administered prior to IRB (1mgkg-1). Six hours of IRB increased phosphorylated p38 in the lung, compared with quietly breathing controls (p = 0.001). Six hours of IRB increased the numbers of macrophages and neutrophils (p = 0.01 and p = 0.005) in BAL fluid. BAL protein levels and lung elasticity increased after both 3 and 6h IRB. TNF-α and MIP-2α increased after 6h of IRB (p = 0.01 and p < 0.001, respectively). Increased lung injury score was detected at 6h IRB. SB203580 administration blocked the increase of neutrophils and macrophages at 6h IRB (p = 0.01 and p = 0.005 to 6h IRB) but not the increase in BAL protein and elasticity. TNF-α, MIP-2α, and injury score at 6h IRB returned to control. p38 activation contributes to IRB-induced pulmonary inflammation.