Airway Occlusion Research Articles

What effect on blood pressure can we expect from continuous positive airway pressure treatment in obstructive sleep apnoea?

What effect on blood pressure can we expect from continuous positive airway pressure treatment in obstructive sleep apnoea?

Comparação de dois métodos de mensuração da pressão inspiratória máxima em pacientes com e sem alterações do nível de consciência

There is no literature consensus about the time of airway occlusion sufficient enough to get a true PImax during weaning from mechanical ventilation (MV). So, the main objectives of the present study were to compare two methods PImax measurement and to evaluate the influence of patients' level of conscience on them. The population was composed by 28 general ICU patients, with MV > 48h, in a weaning process, divided into two groups according to Glasgow coma scale score: with (GCS < 15) and without (GCS = 15) alterations of conscience level. The airway was occluded by using an unidirectional valve for 20s (PImaxT20), or for a maximum time of one minute if a plateau of inspiratory pressure was not observed during three consecutive inspirations (PImaxTid). PImaxT20 (mean ± SD, cmH2O) values were similar in both groups (44 ± 16 vs42 ± 15, p = 0.52). However, PImaxTid values, as long as the time needed to their attainment, were greater in GCS < 15 group (65 ± 24 vs 47 ± 23cmH2O and 37 ± 10 vs24 ± 8s, p = 0.04 and 0.0019, respectively). The method commonly used of 20s airway occlusion seems to be inadequate to get the true PImax in patients with alterations of the level of conscience. Additional studies, now in a more homogeneous group (e. g.: patients with structural brain lesion), are needed to clarify these findings.

Detection of partial endotracheal tube obstruction by forced pressure oscillations

Rapid airway occlusions during mechanical ventilation are followed immediately by high-frequency pressure oscillations. To answer the question if the frequency of forced pressure oscillations is an indicator for partial obstruction of the endotracheal tube (ETT) we performed mathematical simulations and studies in a ventilated physical lung model. Model-derived predictions were evaluated in seven healthy volunteers. Partial ETT obstruction was mimicked by decreasing the inner diameter (ID) of the ETT. In the physical model ETTs of different ID were used. In spontaneously breathing volunteers viscous fluid was applied into the ETT's lumen. According to the predictions derived from mathematical simulations, narrowing of the ETT's ID from 9.0 to 7.0mm decreased the frequency of the pressure oscillations by 11% while changes of the respiratory system's compliance had no effect. In volunteers, a similar reduction (10.9%) was found when 5 ml fluid were applied. We conclude that analysis of pressure oscillations after flow interruption offers a tool for non-invasive detection of partial ETT obstruction.

Olprinone/dopamine combination for improving diaphragmatic fatigue in pentobarbital-anesthetized dogs

Background: Diaphragmatic fatigue might contribute to the development of respiratory failure. In particular, the spontaneous, natural rate of phrenic nerve discharge occurs mainly in low-frequency ranges making low-frequency fatigue clinically important in both humans and animals. Olprinone, a phosphodiesterase 3 inhibitor, improves contractility in fatigued diaphragm, but is also associated with hypotension. Dopamine might be used concomitantly for treating related hypotension. Objective: The purpose of the study was to assess the effect of olprinoneplus dopamine on diaphragmatic fatigue in pentobarbital-anesthetized dogs. Methods: This nonblinded study was conducted at the Department ofAnesthesiology, Institute of Clinical Medicine, Tsukuba, Japan. Diaphragmatic fatigue (assessed by a decrease in diaphragmatic contractility) was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20 Hz applied for 30 minutes. Immediately after the fatigue-producing period, groups 2, 3, and 4 received an initial 10 μg/kg dose of olprinone. Group 2 then received maintenance olprinone of 0.3 μg/kg · min; group 3 received maintenance olprinone 0.3 μg/kg · min plus dopamine 2 μg/kg · min; and group 4 received maintenance olprinone 0.3 μg/kg · min plus dopamine 5 μg/kg · min. Group 1 received no study drug. Olprinone and dopamine were administered IV for 30 minutes. Diaphragmatic contractility was assessed by measuring the maximal transdiaphragmatic pressure (Pdi) generated by test stimuli after airway occlusion at functional residual capacity. Hypotension induced by the study drugs was defined as a >10 mm Hg decrease in mean arterial pressure (MAP), calculated by diastolic pressure plus ⅓ pulse pressure, from baseline. Results: Twenty-eight mongrel dogs (18 males and 10 females, weighing 10-15 kg)were used in the study; 7 dogs were randomly assigned to each treatment group. When fatigue was established in each group, mean (SD) Pdi at low-frequency (20 Hz) stimulation decreased significantly from baseline in all groups (group 1: 15.6 [2.2] vs 11.7 [2.4] cm H 2O, P = 0.008; group 2: 15.4 [1.5] vs 11.6 [1.3] cm H 2O, P= 0.005; group 3:15.5 [2.0] vs 11.6 [1.8] cm H 2O, P= 0.006; group 4: 15.7 [1.4] vs 12.0 [1.4] cm H 2O, P= 0.008), while no significant change existed in Pdi at high-frequency (100 Hz) stimulation ( P = NS). After study drug administration, Pdi in groups 2, 3, and 4 increased significantly from fatigued values at both 20 Hz stimulation (group 2: 11.6 [1.3] vs 21.8 [2.0] cm H 2O, P = 0.001; group 3: 11.6 [1.8] vs 22.2 [1.8] cm H 2O, P = 0.001; group 4: 12.0 [1.4] vs 25.9 [1.9 ] cm H 2O, P = 0.001) and 100 Hz stimulation (group 2: 22.0 [2.2] vs 29.0 [1.9] cm H 2O, P = 0.002; group 3: 22.1 [2.0] vs 29.3 [2.2] cm H 2O, P = 0.002; group 4: 21.8 [2.2] vs 31.7 [2.4] cm H 2O, P= 0.001). The increase in Pdi was significantly larger in group 4 compared with the other 3 groups (all, P < 0.05). Hypotension was not observed in group 4. MAP did not change significantly in group 1 or group 4 compared with baseline or fatigued MAP values ( P = NS). Groups 2 and 3 had significant decreases in MAP with treatment compared with values in group 1 and with baseline and fatigued MAP values (all, P < 0.05). The MAP of group 4 was significantly greater than the MAP of groups 2 and 3 with treatment (both, P < 0.05). Conclusions: Olprinone 0.3 μg/kg sd min plus dopamine 5 μg/kg · min improved contractility in fatigued diaphragms and was not associated with hypotension in these pentobarbital-anesthetized dogs. Olprinone monotherapy and olprinone 0.3 μg/kg · min plus dopamine 2 μg/kg · min might improve contractility significantly. However, it was also associated with significant decreases in MAP.

Hypoxia Impairs the Arousal Response to External Resistive Loading and Airway Occlusion During Sleep

Sustained hypoxia is a neurocognitive depressant, which has been shown to impair respiratory load sensation. Hypoxia has also been shown to impair arousal in animal models, but the effects of sustained hypoxia on arousal in humans have not been studied. The aim of this study was to assess the effects of sustained hypoxia on arousal from sleep in normal subjects. Twelve normal male subjects (age, 24.3 +/- 1.2 years; body mass index, 24.8 +/- 1.4 kg/m2) were studied during stable stage 2 non-rapid eye movement sleep on 2 separate nights 1 week apart. Sleep physiology laboratory. Normal healthy volunteers. Arousal responses to external resistive loads (18 cm H2O x L(-1) x sec(-1)) and occlusions were compared during room-air breathing following sustained normoxia and isocapnic hypoxia (SaO2 approximately 85%). Time to arousal and minimum esophageal pressure preceding arousal were measured. Time to arousal was significantly increased following hypoxia compared with normoxia for resistive loads (24.6 + 4.4 seconds vs. 12.6 +/- 1.9 seconds, p = .007) but not occlusions. Minimum esophageal pressure prior to arousal was more negative following hypoxia for both external loads (-16.8 +/- 1.2 vs. -13.5 +/- 1.3 cm H2O, p = .035) and occlusions (-19.6 +/- 2.2 vs. -15.1 +/- 1.5 cm H2O, p = .029). We conclude that sustained isocapnic hypoxia delays arousal to inspiratory loading during sleep and increases the respiratory arousal threshold. This has implications for disorders characterized by sustained nocturnal hypoxia, such as neuromuscular weakness, chronic obstructive pulmonary disease, obesity-hypoventilation syndrome, and severe obstructive sleep apnea.

Does OSA Distort Perception of Aerobic Exercise Capacity?

Obstructive Sleep Apnea (OSA) is characterized by intermittent nocturnal airway occlusion, sleep fragmentation, and oxygen desaturation. OSA patients report a lower quality of life attributed to excess daytime sleepiness, fatigue, irritability, and impaired cognition. In addition, the great majority of OSA patients are obese and at increased risk for cardiovascular (CV) disease. It has been suggested that this symptom set reduces the perceptions of their ability to engage in and perform physical activities, including participation in aerobic exercise. Thus, encouragement of regular exercise as an adjunct to managing their obesity and excess CV health risks is not seen as viable. PURPOSE: To determine if OSA patients have a distorted perception of their aerobic exercise capacity. METHODS: Forty three sedentary individuals (Mean age ± SD = 36.1 ± 14.4 yr, BMI 31.5 ± 7.9 kg/m2 76% males) with diagnosed OSA [Apnea Hypopnea Index (AHI) = 18.3 ± 13.1 events/hr] were compared to a similar group of 34 controls (27.5 ± 9.4 yr, BMI 28.1 ± 6.1 kg/m2 86% males) without OSA (AHI = 3.2 ± 1.5 events/hr). All were assessed by full overnight laboratory or with at-home polysomnography screening (Medcare, Reykjavik, Iceland). Each completed the Medical Outcomes Study Short Form-36 (SF-36), Veterans Specific Activity Questionnaire (VSAQ), Epworth Sleepiness Scale (ESS), and maximal effort cycle ergometer exercise test using a Δ15W ramping protocol. EPDS, an “Exercise Perception Distortion Score,” [(VO2pk -VO2pk predicted from VSAQ)/VO2pk × 100] was devised to represent distortion in the capability to self-estimate aerobic capacity. RESULTS: OSA and Non-OSA groups did not differ in measured VO2pk or the EPDS. Self-rating of aerobic exercise capacity by age-adjusted VSAQ was highly correlated to VO2pk for the entire sample (n = 77: r = 0.96, p<0.01), and within both the OSA (r = 0.98, p<0.01) and Non-OSA (r = 0.96, p<0.01) groups. The OSA patients reported more sleepiness (ESS, p<0.01), lower physical functioning (PF subscale, p<0.01), and lower role physical scores (RP subscale, p<0.01) than the Non-OSA group. CONCLUSION: Untreated OSA patients perceive themselves as sleepier and less able to engage in low-intensity physical activity. Yet, judgment of their aerobic exercise capacity is accurate and similar to that reported by sedentary individuals without OSA. These results encourage further research to evaluate the efficacy of moderate-vigorous exercise as an adjunct to medical management of CV disease risks in OSA patients. Supported by a grant from ResMed Sleep Disordered Breathing Foundation, Poway, CA.

Plethysmographic estimation of thoracic gas volume in apneic mice

Electrical stimulation of intercostal muscles was employed to measure thoracic gas volume (TGV) during airway occlusion in the absence of respiratory effort at different levels of lung inflation. In 15 tracheostomized and mechanically ventilated CBA/Ca mice, the value of TGV obtained from the spontaneous breathing effort available in the early phase of the experiments (TGVsp) was compared with those resulting from muscle stimulation (TGVst) at transrespiratory pressures of 0, 10, and 20 cmH2O. A very strong correlation (r2= 0.97) was found, although with a systematically (approximately 16%) higher estimation of TGVst relative to TGVsp, attributable to the different durations of the stimulated (approximately 50 ms) and spontaneous (approximately 200 ms) contractions. Measurements of TGVst before and after injections of 0.2, 0.4, and 0.6 ml of nitrogen into the lungs in six mice resulted in good agreement between the change in TGVst and the injected volume (r2= 0.98). In four mice, TGVsp and TGVst were compared at end expiration with air or a helium-oxygen mixture to confirm the validity of isothermal compression in the alveolar gas. The TGVst values measured at zero transrespiratory pressure in all CBA/Ca mice [0.29 +/- 0.05 (SD) ml] and in C57BL/6 (N = 6; 0.34 +/- 0.08 ml) and BALB/c (N = 6; 0.28 +/- 0.06 ml) mice were in agreement with functional residual capacity values from previous studies in which different techniques were used. This method is particularly useful when TGV is to be determined in the absence of breathing activity, when it must be known at any level of lung inflation or under non-steady-state conditions, such as during pharmaceutical interventions.

Intraatrial extension of thyroid cancer: a case report.

A 61-year-old man, who was diagnosed with superior vena cava syndrome by papillary thyroid carcinoma, was referred to our hospital. A bulky thyroid tumor with tracheal invasion extended from the left neck to the right atrium without distant metastases. The risk of sudden death due to airway occlusion, tumor embolism or obstruction of the tricuspid valve led us to elect surgery. Extended resection of thyroid cancer was performed with cardiopulmonary bypass. Peritoneal dissemination was found via laparotomy. A histological diagnosis of anaplastic carcinoma arising from transformation of papillary carcinoma was made. After the operation, bilateral ureteral occlusion by peritoneal dissemination and multiple lung metastases were detected. The patient died with acute renal failure on postoperative day 12. Intraatrial extension of thyroid cancer is rare, and only 12 cases have been reported in the literature. We present a case of thyroid cancer with intraatrial extension.

Brief Airway Occlusion Produces Prolonged Reflex Inhibition of Inspiratory Muscles in Obstructive Sleep Apnea

The human inspiratory muscles respond to a brief occlusion of the upper airway during inspiration with a profound short-latency reflex inhibition. This inhibition contrasts with the excitatory stretch reflex of limb muscles and may protect the airway from aspiration. It was postulated that this reflex would be altered in subjects with obstructive sleep apnea (OSA) who have repetitive upper airway occlusion. Subjects underwent overnight polysomnography, as well as muscle reflex studies. For the reflex studies (performed during wakefulness), occlusions lasting 250 milliseconds were delivered during inspiration. Surface electromyogram was recorded over the scalenes, parasternal intercostals, and chest wall (overlying diaphragm). Research and sleep laboratories. Nineteen subjects with untreated OSA (9 moderate and 10 severe) and 9 healthy control subjects. In the subjects with severe OSA, the duration of the inhibition was prolonged by at least 25% compared with control subjects. The peak of the inhibitory response for scalenes occurred significantly later for subjects with severe OSA than for control subjects (by 76 +/- 5 ms vs 60 +/- 3 ms [mean +/- SEM], respectively). Onset latencies of the later excitatory response were delayed for scalenes, parasternal intercostals, and chest wall recordings (eg, scalenes: 105 +/- 9 ms for subjects with severe OSA vs 83 +/- 5 ms for control subjects). The latency of peak inhibition and duration of inhibition were positively correlated with the respiratory disturbance index for all muscle groups. These changes may reflect adaptation in central respiratory paths due to repetitive loading during sleep.

Mechanism of Expiratory Muscle Activation During Upper Lumbar Spinal Cord Stimultion (SCS)

Combined lower thoracic (T9) and upper lumbar (L1) SCS may be a useful method to restore an effective cough mechanism in tetraplegic patients. In previous studies in dogs, we demonstrated that SCS at the T9 level resulted in direct activation of the spinal cord roots in the vicinity of the stimulating electrode and also more caudal roots via spinal pathways. The purpose of the present study was to investigate the mechanism of expiratory muscle activation during upper lumbar (L1) SCS. In 3 anesthetized dogs, expiratory muscle activation was monitored by evoked compound action potentials (CAP) from the intercostal muscles in the 7th and 9th interspaces (T7, T9) and portions of the external oblique innervated by the T13 and L2 motor roots. SCS applied with single shocks resulted in short latency CAP at T13 and L2 but not more rostrally. SCS resulted in long latency CAPs at T7 and T9, suggesting activation via spinal cord pathways. SCS at L1 was also applied before and after sequential section of the dorsal columns (DC), lateral (LF) and ventral funiculi (VF) at the T11 spinal cord level while monitoring airway pressure under conditions of airway occlusion. DC section did not affect short latency CAPs but abolished long latency CAPs at T9 and T7 and also resulted in a fall in airway pressure generation from 26 ± 6 cmH2O to 18 ± 5 cmH2O (NS). Section of the LF and VF resulted in further decrements in airway pressure (17 ± 6 and 11 ± 2 cmH2O respectively, NS). We conclude that SCS at the L1 level results in direct activation of the spinal roots in the vicinity of stimulating electrode and more rostral roots via spinal pathways. (HL34143).

Esophageal Causes of Sudden and Unexpected Death

Gastrointestinal conditions are uncommon causes of sudden and/or unexpected death as compared to cardiovascular diseases, motor vehicle trauma, or suicide, and may involve an array of fatal mechanisms. Lethal esophageal conditions are encountered even less often, the manifestations of which include acute upper airway occlusion from tumors or foreign material, intraluminal hemorrhage from vascular abnormalities, or perforation with fistula formation resulting in hemorrhage and sepsis. When encountered at autopsy, a particular condition may also be a manifestation of a disease that does not primarily involve the esophagus. For this reason, a detailed autopsy investigation is required for evidence of systemic or remote disease when lesions are found within the esophagus. In this report, possible life-threatening esophageal conditions are reviewed with a description of lethal mechanisms, mention of rare associated diseases, and comment on difficulties that may arise at autopsy in the evaluation of such cases.

Cardiovascular Effects of Chronic Intermittent Hypoxia in Mice

Obstructive sleep apnea syndrome (OSA), resulting from repetitive episodes of upper airway occlusion during sleep, increases cardiovascular mortality and morbidity. To determine suitability of mouse model for OSA, we examine the cardiovascular response to chronic intermittent hypoxia (CIH), one of major physiological changes in OSA. Methods Adult C57BL/6 mice were daily exposed to either CIH (cycles of 1-min hypoxia with nadir FIO2 5%, followed by 1-min normoxia, 10 daytime hours/day for 2 months, n=22) or similarly handled normoxic control (C, n=17). Measurements performed include body weight (BW); cardiac catheterization under 2% isoflurane anesthesia after 12 hours following the end of the last exposure; and heart wet weight after euthanasia. Results There is no significant difference between CIH and C in BW, heart rate, rate of left ventricular (LV) pressure rise (+dP/dtmax), rate of LV pressure fall (−dP/dtmax), and weight ratio of right ventricular free wall to BW. CIH increased mean arterial pressure (CIH: 92.8±11.7 vs C: 84.5±11.5 mm Hg, p=0.03), LV end-diastolic pressure (12.5±6.8 vs 5.5±5.4 mm Hg, p<0.01), heart weight to BW ratio (4.1±0.6 vs 3.6±0.3 mg/g, p<0.05), and LV free wall weight to BW ratio (2.07±0.27 vs 1.71±0.18 mg/g, p<0.01). Conclusions Mice with CIH develop higher blood pressure, LV dysfunction, and LV hypertrophy. These changes mimic cardiovascular changes in patients with OSA. We speculate that future use of genetically modified mice with CIH may be useful for investigation of the molecular mechanisms of cardiovascular change in OSA. Supported by NHLBI.

Amelioration of Influenza-Induced Pathology in Mice by Coinfection withTrichinella spiralis

Illness due to respiratory virus infection is often induced by excessive infiltration of cells into pulmonary tissues, leading to airway occlusion. We show here that infection with Trichinella spiralis results in lower levels of tumor necrosis factor in bronchoalveolar lavage fluid and inhibits cellular recruitment into the airways of mice coinfected with influenza A virus. Infiltration of neutrophils and CD4+ and CD8+ lymphocytes was reduced, resulting in animals gaining weight more rapidly following the initial phase of infection. Influenza resulted in a generalized increase in vascular permeability in pulmonary tissues, and this was suppressed by parasite infection, although the effects were restricted to the early phase of trichinosis. Moreover, the number of cells producing interleukin-10 (IL-10), and the local levels of this cytokine, were reduced, suggesting that amelioration of pulmonary pathology by parasite infection occurs independently of IL-10 production.

Effects of Lung Squeezing Technique on Lung Mechanics in Mechanically-Ventilated Preterm Infants with Respiratory Distress Syndrome

Effects of conventional chest physiotherapy on preterm infants may be compromised due to the maturation difference in immature lungs. The lung squeezing technique (LST) has been shown to be beneficial in correcting atelectasis in preterm infants. The purpose of this study was to investigate the effects of LST on the parameters of lung mechanics in preterm infants on mechanical ventilation. LST was used as an intervention to improve the distribution of ventilation in infants with respiratory distress syndrome. Eleven preterm infants on mechanical ventilation were enrolled. Serial measurements on static respiratory system compliance (Crs) and resistance (Rrs) by an airway occlusion technique with passive flow-volume analysis were performed before and immediately after LST, and repeated 4 hours later to assess the carryover effect. Crs improved by 21% (0.92 ± 0.37 mL/cmH 2 O/kg vs. baseline 0.76 ± 0.33 mL/cmH 2 O/kg, p = 0.023) immediately after LST. Split group analysis showed that only the lower Crs group had a significant carryover effect at 4 hours post-LST (p = 0.046). LST increases total respiratory system compliance, possibly through decompression of the overdistended lung units and recruitment of atelectatic alveoli. Rrs showed no significant change after LST. Individual trends of decreased Rrs were observed in infants with obvious secretion. The effect of LST on respiratory system resistance needs to be further explored by recruiting other disease conditions that present with pulmonary secretions.

Stereotactic body radiation therapy for centrally located lung lesions

Presentation of outcomes of patients treated by stereotactic body radiation therapy (SBRT) for lung lesions located within or touching a 2 cm zone around major airways. Serial tomotherapeutic SBRT has been planned and delivered at our institution since August 2001. Of 108 patients treated for primary and secondary lung tumors, nine harbored tumors (8 metastases, 1 recurrent NSCLC) located in close proximity to carina, right and left main bronchi, right and left upper lobe bronchi, intermedius, right middle lobe, lingular, or right and left lower lobe bronchi. SBRT was delivered to total doses of 36 Gy in 3 fractions (n = 8) or 6 fractions (n = 1), using a serial tomotherapy system (Nomos Peacock). We assessed local tumor control, clinical toxicity, normal tissue imaging changes, and overall survival. Median tumor volume was 26 cm3 (range 1.7 to 135 cm3). Tumor locations were hilar (n = 3), and parenchymal in six cases. Hilar lesions accounted for the three largest tumor volumes in the series. During a median follow-up of 10.6 months (range 2.5 to 41.5 months), all lesions treated were locally controlled as confirmed by CT or CT/PET imaging. Parenchymal imaging changes included focal lung fibrosis and major airway wall thickening. One occurrence of major airway occlusion (right lower lobe bronchus) was observed. This event was diagnosed by chest x-ray at 36 months, following treatment of the second largest hilar lesion in the present series. Based on the outcomes observed in this small sample series, SBRT for centrally located lung lesions appears feasible, was associated with low incidence of toxicities, and provided sustained local tumor control. However, long-term survival may be associated with major airway injury. As long-term follow-up in larger numbers of patients is lacking at this time, exclusion of patients with centrally located lesions may be considered when patients are treated in curative intent.

Extraluminal tissue pressure: what does it mean?

In this issue of the Journal of Applied Physiology , Kairaitis et al. ([9][1]) examine the control of pharyngeal extraluminal tissue pressure by mandibular advancement and jaw position. Utilizing a novel approach for measuring peripharyngeal tissue pressures, they demonstrated that mandibular

Café coronary syndrome-fatal choking on food: An autopsy approach

To examine the characteristic features of fatal food asphyxia and to develop an autopsy approach to such cases a retrospective study of autopsy files was undertaken at Forensic Science SA (Adelaide, Australia) over a 10 year period from 1993 to 2002 for all cases of food asphyxia/café coronary syndrome. Forty-four cases were identified (M;F = 21:23), with one infant (11 mths) and 43 adults (30–96 yrs; mean 68.9 yrs), with a preponderance of victims (57%) aged between 71 and 90 yrs. Deaths occurred in nursing homes ( N = 22) cases, at home ( N = 11) and in restaurants ( N = 4). Twenty-seven of the victims (61%) had histories of neurological or psychiatric disorders such as dementia ( N = 8), schizophrenia ( N = 6), Alzheimer disease ( N = 4), atherosclerotic cerebrovascular disease ( N = 4), mental impairment ( N = 2), multiple sclerosis ( N = 1), Parkinson disease ( N = 1) and obsessive-compulsive disorder ( N = 1). Twenty-seven cases (61%) were described as either edentulous or having significant numbers of teeth missing. Toxicological evaluation of blood revealed alcohol and a variety of psychotropic prescription medications in 19 cases. Sudden collapse during or shortly after a meal should always raise the possibility of café coronary and the autopsy examination should not only attempt to demonstrate airway occlusion by a bolus of food, but also to identify or exclude underlying neurological disease. Such cases may raise issues concerning adequacy of care and appropriateness of medication. The diagnosis of café coronary syndrome can only be made with confidence after the clinical history and circumstances of death have been clearly established, impacted material has been demonstrated in the airway at autopsy (or recorded by those attempting resuscitation), risk factors have been identified and other possible causes of death have been excluded.

Optimal arrangement of magnetic coils for functional magnetic stimulation of the inspiratory muscles in dogs

In an attempt to maximize inspiratory pressure and volume, the optimal position of a single or of dual magnetic coils during functional magnetic stimulation (FMS) of the inspiratory muscles was evaluated in twenty-three dogs. Unilateral phrenic magnetic stimulation (UPMS) or bilateral phrenic magnetic stimulation (BPMS), posterior cervical magnetic stimulation (PCMS), anterior cervical magnetic stimulation (ACMS) as well as a combination of PCMS and ACMS were performed. Trans-diaphragmatic pressure (Pdi), flow, and lung volume changes with an open airway were measured. Transdiaphragmatic pressure was also measured with an occluded airway. Changes in inspiratory parameters during FMS were compared with 1) electrical stimulation of surgically exposed bilateral phrenic nerves (BPES) and 2) ventral root electrical stimulation at C5-C7 (VRES C5-C7). Relative to the Pdi generated by BPES of 36.3 +/- 4.5 cm H2O (Mean +/- SEM), occluded Pdi(s) produced by UPMS, BPMS, PCMS, ACMS, and a combined PCMS + ACMS were 51.7%, 61.5%, 22.4%, 100.3%, and 104.5% of the maximal Pdi, respectively. Pdi(s) produced by UPMS, BPMS, PCMS, ACMS, and combined ACMS + PCMS were 38.0%, 45.2%, 16.5%, 73.8%, and 76.8%, respectively, of the Pdi induced by VRES (C5-C7) (48.0 +/- 3.9 cm H2O). The maximal Pdi(s) generated during ACMS and combined PCMS + ACMS were higher than the maximal Pdi(s) generated during UPMS, BPMS, or PCMS (p < 0.05). ACMS alone induced 129.8% of the inspiratory flow (73.0 +/- 9.4 L/ min) and 77.5% of the volume (626 +/- 556 ml) induced by BPES. ACMS and combined PCMS + ACMS produce a greater inspiratory pressure than UPMS, BPMS or PCMS. ACMS can be used to generate sufficient inspiratory pressure, flow, and volume for activation of the inspiratory muscles.

Respiratory muscle performance with stretch‐shortening cycle manoeuvres: maximal inspiratory pressure–flow curves

To test the hypothesis that the maximal inspiratory muscle (IM) performance, as assessed by the maximal IM pressure-flow relationship, is enhanced with the stretch-shortening cycle (SSC). Maximal inspiratory flow-pressure curves were measured in 12 healthy volunteers (35 +/- 6 years) during maximal single efforts through a range of graded resistors (4-, 6-, and 8-mm diameter orifices), against an occluded airway, and with a minimal load (wide-open resistor). Maximal inspiratory efforts were initiated at a volume near residual lung volume (RV). The subjects exhaled to RV using slow (S) or fast (F) manoeuvres. With the S manoeuvre, they exhaled slowly to RV and held the breath at RV for about 4 s prior to maximal inspiration. With the F manoeuvre, they exhaled rapidly to RV and immediately inhaled maximally without a post-expiratory hold; a strategy designed to enhance inspiratory pressure via the SSC. The maximal inspiratory pressure-flow relationship was linear with the S and F manoeuvres (r2 = 0.88 for S and r2 = 0.88 for F manoeuvre, P < 0.0005 in all subjects). With the F manoeuvre, the pressure-flow relationship shifted to the right in a parallel fashion and the calculated maximal power increased by approximately 10% (P < 0.05) over that calculated with the S manoeuvre. The maximal inspiratory pressure-flow capacity can be enhanced with SSC manoeuvres in a manner analogous to increases in the force-velocity relationship with SSC reported for skeletal muscles.

Mast cells protect mice from Mycoplasma pneumonia.

As the smallest free-living bacteria and a frequent cause of respiratory infections, mycoplasmas are unique pathogens. Mice infected with Mycoplasma pulmonis can develop localized, life-long airway infection accompanied by persistent inflammation and remodeling. Because mast cells protect mice from acute septic peritonitis and gram-negative pneumonia, we hypothesized that they defend against mycoplasma infection. This study tests this hypothesis using mast cell-deficient mice. Responses to airway infection with M. pulmonis were compared in wild-type and mast cell-deficient Kit(W-sh)/Kit(W-sh) mice and sham-infected control mice. Endpoints include mortality, body and lymph node weight, mycoplasma antibody titer, and lung mycoplasma burden and histopathology at intervals after infection. The results reveal that infected Kit(W-sh)/Kit(W-sh) mice, compared with other groups, lose more weight and are more likely to die. Live mycoplasma burden is greater in Kit(W-sh)/Kit(W-sh) than in wild-type mice at early time points. Four days after infection, the difference is 162-fold. Titers of mycoplasma-specific IgM and IgA appear earlier and rise higher in Kit(W-sh)/Kit(W-sh) mice, but antibody responses to heat-killed mycoplasma are not different compared with wild-type mice. Infected Kit(W-sh)/Kit(W-sh) mice develop larger bronchial lymph nodes and progressive pneumonia and airway occlusion with neutrophil-rich exudates, accompanied by angiogenesis and lymphangiogenesis. In wild-type mice, pneumonia and exudates are less severe, quicker to resolve, and are not associated with increased angiogenesis. These findings suggest that mast cells are important for innate immune containment of and recovery from respiratory mycoplasma infection.