Airway Occlusion Research Articles

Effects on Respiratory Mechanics of Bronchoalveolar Lavage in Mechanically Ventilated Patients

Inconsistent findings have been reported about the effects of bronchoalveolar lavage (BAL) on respiratory mechanics. The aims of this study were to study the effects of BAL on respiratory mechanics in mechanically ventilated patients with suspected pneumonia and to find out whether these effects are related to the extension of radiographic infiltrate and preceding respiratory mechanics measurements. Bronchoscopy BAL was performed with 150 mL of sterile isotonic saline in 3 aliquots of 50 mL. Respiratory mechanics parameters were measured by the rapid airway occlusion technique, immediately before and after BAL and 90 minutes later. Patients were classified according to unilateral or bilateral radiological infiltrate occurrence. Fifty critically ill patients undergoing mechanical ventilation were included. Respiratory system compliance (Crs) decreased from 43.32±13.17 mL/cm H2O to 33.02±9.56 mL/cm H2O (P<0.01) and airway resistance increased from 15.16±7.04 cm H2O/L/s to 17.54±9.40 cm H2O/L/s (P<0.05) immediately after BAL; 90 minutes later both the parameters returned to the pre-BAL values. Patients who showed a greater than 20% decrease in Crs had a higher pre-BAL Crs than patients with a less severe decrease (49.85±10.7 mL/cm H2O vs. 35.65±11.67 mL/cm H2O; P<0.01). However, neither pre-BAL airway resistance nor the extension of the radiographic infiltrates was related to the changes in respiratory mechanics. BAL in mechanically ventilated patients can lead to a significant, although transitory, deterioration in pulmonary mechanics, characterized by a decrease in Crs and by an increase in airway resistance. Patients with better initial Crs showed the most severe affectation.

Historical changes in perspective of the etiology, pathophysiology and treatment of obstructive sleep apnea

NOTE: This is a History of Medicine submission and does not have an abstract. As such the Introduction section has been pasted here as an abstract. Obstructive sleep apnea (OSA) is a condition characterized by repeated occlusion of the upper airway (UA) during sleep. From OSA’s initial clinical description less than 50 years ago to present day, progression in respiratory sleep medicine has vastly expanded the scope of our knowledge of OSA. What was once regarded as a rare affliction that simply led to daytime hypersomnelence1 is now recognized as a common and serious condition capable wreaking havoc in the cardiovascular system, independently promoting heart failure, stroke, hypertension and likely atherosclerosis.At the beginning of a new decade, the field of OSA research finds itself at yet another frontier as a radically new etiological perspective emerges. This new paradigm of the cause of OSA promises the possibility of novel OSA treatments and prophylaxes. This article will follow the progression of OSA research, from the condition's initial discovery, on to the current widely-accepted view of OSA and finally to the future of respiratory sleep medicine.

Treatment of mucous hypersecretion

SummaryAirway secretions are produced by glandular and epithelial exocytosis and vascular permeability. Each process plays a unique role in different disease states, and so treatment must be tailored to the pathophysiological mechanism(s). In acute allergic rhinitis, the watery rhinorrhea is predominantly plasma with only about one‐third derived from histamine‐induced nociceptive afferent nerve and parasympathetic reflexes. The acetylcholine acts on muscarinic M3 receptors on glands to stimulate exocytosis from both mucous and serous cells. Parasympathetic, cholinergic reflex‐mediated glandular secretion responds very well to anticholinergic drugs. More chronic inflammation as seen in chronic rhinosinusitis and bronchitis leads to goblet cell hyperplasia and increased secretion of mucin 5AC (MUC5AC), a secreted, gel‐forming mucin that contains many serine–threonine repeats that are studded with large O‐linked carbohydrate groups. Progressively worsening inflammation leads to the addition of sialic acid and sulphate to generate acidic mucins. The protein chains are cross‐linked by disulphide bonds to form large, buoyant islands that float on the epithelial lining fluid. These sticky macromolecules form complexes with albumin and neutrophil‐derived DNA, F‐actin, and proteolytic enzymes, creating mucoclots. These tenacious, viscous, mucoclots can adhere to epithelial linings, which may lead to occlusion of small airways that causes reduced airflow in chronic obstructive pulmonary disease and asthma. Mucous plugging is a problem leading to the overwhelming mucous hypersecretion and solidification of ‘end‐stage’ acute asthma attacks. Mucous hypersecretion of this severity has been correlated with increased morbidity and mortality in lung disease. Anticholinergic drugs are essential therapies in these conditions. Other medications for mucous hypersecretion include expectorants, anti‐inflammatory agents, macrolides, inhaled DNase, and a host of unproven products. Information about signal transduction, transcriptional regulation, and mucin synthesis has provided a framework for understanding the excess production of goblet cell MUC5AC in disease, and has identified potential targets for future drug therapy.

Isolated invasive Aspergillus tracheobronchitis: a clinical study of 19 cases

Isolated invasive Aspergillus tracheobronchitis (iIATB) is an uncommon clinical form of invasive Aspergillosis in which Aspergillus infection is limited entirely or predominantly to the tracheobronchial tree. In the present study, we retrospectively analyzed the medical records of 19 patients who had histological documented iIATB in the Department of Respiratory Medicine of Changhai Hospital between October 2000 and February 2008. Malignancy was the most common underlying disease, which existed in 14 patients (73.7%) in our series. Most patients had impaired airway structures or defence functions, whereas the systemic immune status was relatively normal. Only three patients (15.8%) had neutropenia. The clinical manifestations and chest radiograph were non-specific. We classified iIATB into four different forms according to the bronchoscopic features of intraluminal lesions: superficial infiltration type (Type I, n = 4), full-layer involvement type (Type II, n = 2), occlusion type (Type III, n = 6) and mixed type (Type IV, n = 7). Type IV was the largest group in our study, followed by Type III. All patients with iIATB of Type IV had definite airway occlusion. Fourteen patients (73.7%) had a good response to antifungal treatments and five (26.3%) died as a result of the progression of Aspergillosis, all of whom had full-layer invasion of the involved bronchi. In conclusion, we found that iIATB could occur in moderately or non-immunocompromised patients with impaired airway structures or defence functions and may be an early period of invasive pulmonary Aspergillosis. Most of the iIATB patients had a favourable prognosis with early diagnosis and effective antifungal treatment. The morphological features of intraluminal lesions might be of prognostic value.

Suspension of DNR: Ethical Considerations in the Perioperative Arena

The amazing thyroid gland is an integral part of the endocrine system within the human body. This butterfly shaped gland is located anterior to the larynx and produces the hormones Throxine (T3), Triiodothyronine (T4), and Calcitonin. Surgical removal is indicated when medical treatment fails or when cancer is suspected. Preoperative nursing care is critical for positive outcomes throughout the surgical continuum. The preoperative nurse must complete a thorough assessment of both physical and psychosocial facets with the patient. Physical assessment should include: any signs of a hypermetabolic state, any cervical disk disease or injury that may impede positioning of the patient in the OR, voice quality should be documented so nerve injury can be detected quickly in the post operative period, and any dysphasia or neck swelling should be noted. Psychosocial considerations may include fear of surgery or concern about the cosmetic outcome. Patient support and education can allay many fears. Post-operative complications may include airway occlusion, bleeding, laryngeal nerve injury, hypocalcemia, and parathyroid deficit. Infrequent post operative complications include sympathetic nerve injury, infection, and thyroid storm. Patients can be reassured that their safety, needs, and concerns are met with professional perianesthesia care.

Mesenchymal stem cells reduce inflammation in a rat model of obstructive sleep apnea

The aim was to test the hypothesis that mesenchymal stem cells (MSC) could reduce the inflammation induced by recurrent airway occlusions in an animal model of obstructive sleep apnea (OSA). A nasal mask was applied to 30 anesthetized rats. Twenty rats were subjected to a pattern of recurrent obstructive apneas mimicking OSA (60/h, lasting 15 s each) for 5h. MSC (5x10(6) cells) were intravenously injected into 10 of these rats. Ten rats not subjected to apneas or MSC injection were used as controls. The rat blood serum concentrations of pro-inflammatory cytokine IL-1beta were measured by ELISA. IL-1beta was significantly greater in the rats subjected to recurrent apneas (66.7+/-41.2 pg/mL; m+/-SEM) than in controls (1.9+/-1.0 pg/mL; p<0.05). In the group of apneic rats subjected to MSC injection, IL-1beta was significantly reduced (6.1+/-3.8 pg/mL; p<0.05). In conclusion, MSC triggered an early anti-inflammatory response in rats subjected to recurrent obstructive apneas, suggesting that these stem cells could play a role in the physiological response to counterbalance inflammation in OSA.

Increased Expression of Angiopoietins and Tie2 in the Lungs of Chronic Asthmatic Mice

Angiopoietin (Ang)1 and Ang2 are ligands for Tie2 tyrosine kinase receptor (Tie2). Elevated levels of Ang1 and Ang2 in induced sputum of patients with asthma have been reported, with a positive correlation of Ang2 levels with the severity of airway occlusion. Although studies have shown Tie2-mediated regulation of nonvascular cells in some pathological conditions, current knowledge on Tie2 signaling in asthma is limited to the vasculature. We examined the expression pattern of Ang1, Ang2, vascular endothelial growth factor (VEGF), and Tie2 and their correlation with the degree of airway remodeling in the lung of ovalbumin (OVA)-sensitized and OVA-challenged mice with airway hyperresponsiveness. Lung tissues were isolated from Balb/c mice after OVA sensitization and challenge. Hematoxylin and eosin, periodic acid-Schiff, and trichrome staining were used to show the lung pathology. The expression of Ang1, Ang2, VEGF, and Tie2 was examined using immunofluorescence, Western blot, ELISA, and real-time PCR. In the lung of normal mice, Tie2 expression was detected only in the blood vessels. However, in the lung of OVA-sensitized and OVA-challenged mice, Tie2 was abundantly expressed in airway epithelial cells and in a subset of macrophages in addition to constitutive expression in pulmonary vessels. The increase in Tie2 expression correlated with the severity of airway remodeling. Macrophages and airway epithelial cells express Ang2 and VEGF only in allergic models. Ang1 was constitutively expressed, with a decrease in mRNA level in allergic models. In conclusion, increased expression of Tie2 and Ang2 in allergic airway epithelium and alveolar macrophages correlates with the severity of airway remodeling.

Association of circulating angiotensin converting enzyme activity with respiratory muscle function in infants

BackgroundAngiotensin converting enzyme (ACE) gene contains a polymorphism, consisting of either the presence (I) or absence (D) of a 287 base pair fragment. Deletion (D) is associated with increased circulating ACE (cACE) activity. It has been suggested that the D-allele of ACE genotype is associated with power-oriented performance and that cACE activity is correlated with muscle strength. Respiratory muscle function may be similarly influenced. Respiratory muscle strength in infants can be assessed specifically by measurement of the maximum inspiratory pressure during crying (Pimax). Pressure-time index of the respiratory muscles (PTImus) is a non-invasive method, which assesses the load to capacity ratio of the respiratory muscles.The objective of this study was to determine whether increased cACE activity in infants could be related to greater respiratory muscle strength and to investigate the potential association of cACE with PTImus measurements as well as the association of ACE genotypes with cACE activity and respiratory muscle strength in this population.MethodsSerum ACE activity was assayed by using a UV-kinetic method. ACE genotyping was performed by polymerase chain reaction amplification, using DNA from peripheral blood. PTImus was calculated as (Pimean/Pimax) × (Ti/Ttot), where Pimean was the mean inspiratory pressure estimated from airway pressure, generated 100 milliseconds after an occlusion (P0.1), Pimax was the maximum inspiratory pressure and Ti/Ttot was the ratio of the inspiratory time to the total respiratory cycle time. Pimax was the largest pressure generated during brief airway occlusions performed at the end of a spontaneous crying effort.ResultsA hundred and ten infants were studied. Infants with D/D genotype had significantly higher serum ACE activity than infants with I/I or I/D genotypes. cACE activity was significantly related to Pimax and inversely related to PTImus. No association between ACE genotypes and Pdimax measurements was found.ConclusionsThese results suggest that a relation in cACE activity and respiratory muscle function may exist in infants. In addition, an association between ACE genotypes and cACE activity, but not respiratory muscle strength, was demonstrated.

Not sleeping well can damage your heart

Obstructive sleep apnea (OSA) is characterized by recurrent obstruction of the pharyngeal airway during sleep, and results in episodes of intermittent hypoxia. Regardless of the presence of daytime symptoms, OSA is an independent risk factor for cardiovascular disease and increased mortality.1 A number of studies have shown that development of OSA correlates with increasing weight. The prevalence of OSA among obese patients has been reported, and substantial improvement was achieved by weight reduction.2 Regarding the pathophysiology of OSA, an anatomically small pharyngeal airway is a prerequisite factor leading to OSA. This smaller airway size always worsens with increasing body fat and obesity.3 When luminal size is narrower, it makes the airway vulnerable to collapse. An individual with OSA is able to compensate for this modified anatomy by increasing the activity of the upper airway muscles during the time that he or she is awake. However, with the onset of sleep, this compensation is lost and airway obstruction occurs. Even short periods of apnea can induce a rise in PaCO2, a fall in PaO2, and increased ventilatory effort against an occluded airway. Therefore, patients with OSA experience repetitive episodes of hypoxia during transient cessation of breathing that promote inflammation and oxidative stress. In addition to direct fat deposits within the airway walls, the upper airway size may be smaller in obese patients because of a reduced lung volume.3

Small dead space heat and moisture exchangers do not impede gas exchange during noninvasive ventilation: a comparison with a heated humidifier

Adverse respiratory and gasometrical effects have been described in patients with acute respiratory failure (ARF) undergoing noninvasive ventilation (NIV) with standard heat and moisture exchangers (HME). We decided to evaluate respiratory parameters and arterial blood gases (ABG) of patients during NIV with small dead space HME compared with heated humidifier (HH). Prospective randomized crossover study. A 16-bed medical intensive care unit (ICU). Fifty patients receiving NIV for ARF. The effects of HME and HH on respiratory rate, minute ventilation, EtCO(2), oxygen saturation, airway occlusion pressure at 0.1 s, ABG, and comfort perception were compared during two randomly determined NIV periods of 30 min. The relative impact of HME and HH on these parameters was successively compared with or without addition of a flex tube (40 and 10 patients, respectively). No difference was observed between HME and HH regarding any of the studied parameters, whether or not a flex tube was added. If one decides to humidify patients' airways during NIV, one may do so with small dead space HME or HH without altering respiratory parameters.

A secondary reflex suppression phase is present in genioglossus but not tensor palatini in response to negative upper airway pressure.

On the basis of recent reports, the genioglossus (GG) negative-pressure reflex consists initially of excitation followed by a secondary state-dependent suppression phase. The mechanistic origin and functional role of GG suppression is unknown but has been hypothesized to arise from transient inhibition of respiratory active neurons as a protective reflex to prevent aspiration, as observed in other respiratory muscles (e.g., diaphragm) during airway occlusion. Unlike GG, tensor palatini (TP) is a tonic muscle with minimal respiratory phasic activation during relaxed breathing, although both muscles are important in preserving pharyngeal patency. This study aimed to compare GG vs. TP reflex responses to the same negative-pressure stimulus. We hypothesized that reflex suppression would be present in GG, but not TP. Intramuscular GG and TP EMGs were recorded in 12 awake, healthy subjects (6 female). Reflex responses were generated via 250-ms pulses of negative upper airway pressure (approximately -16 cmH2O mask pressure) delivered in early inspiration. GG and TP demonstrated reflex activation in response to negative pressure (peak latency 31+/-4 vs. 31+/-6 ms and peak amplitude 318+/-55 vs. 314+/-26% baseline, respectively). A secondary suppression phase was present in 8 of 12 subjects for GG (nadir latency 54+/-7 ms, nadir amplitude 64+/-6% baseline), but not in any subject for TP. These data provide further support for the presence of excitatory and inhibitory components of GG (phasic muscle) in response to brief upper airway negative-pressure pulses. Conversely, no reflex suppression below baseline was present in TP (tonic muscle) in response to the same stimuli. These differential responses support the hypothesis that GG reflex suppression may be mediated via inhibition of respiratory-related premotor input.

Case Scenario: Perioperative Airway Management of a Patient with Tracheal Stenosis

TRACHEAL stenosis is a rare but a life-threatening condition and is caused by congenital problems, postintubation injury, trauma, tracheal tumor, and compression of the trachea by tumor. Although accurate prevalence of this condition is unknown, an incidence of 4.9 cases per million per year is estimated for postintubation tracheal stenosis. A stenosis commonly occurs at the cuff of the tube (intrathoracic trachea) or at the level of the tracheostomy stoma (extrathoracic trachea). Anesthesia of a patient with tracheal stenosis is challenging for anesthesiologists. Depending on the severity and location of the stenosis and the type of surgical procedure, there may be a variety of choices for perioperative airway management such as a facemask, laryngeal mask airway, an tracheal intubation tube, cardiopulmonary bypass, and extracorporeal membrane oxygenation. The American Society of Anesthesiologists practice guidelines for management of the difficult airway primarily focus airway problems caused at the extrathoracic airway and may not be helpful, particularly for managing patients with intrathoracic tracheal stenosis. In this case scenario, we present a patient with severe intrathoracic tracheal stenosis, who required surgery for a lumbar fracture in the prone position. Various airway management strategies and the actual management used are discussed.

It's Not All Smooth Muscle: Non-Smooth-Muscle Elements in Control of Resistance to Airflow

To achieve gas exchange, inspired air must pass through an intricate and dynamic tracheobronchial tree. The tree offers resistance to airflow, and increased resistance is the most important functional change in lung disease. Numerous mechanisms contribute to increased resistance by causing airway narrowing, closure, occlusion, and/or obliteration. Although airway smooth muscle (ASM) contraction and shortening are an important cause of increased resistance, non-ASM elements can also contribute. Nonmuscle elements can modify the amount of airway narrowing for any given level of ASM shortening and the amount of shortening for a given level of ASM activation. In this review, we outline the physiological basis for airflow resistance and describe how changes in the lung parenchyma, the airways, and their luminal contents can contribute to increased airflow resistance. A detailed understanding of the mechanisms and consequences of increased airway resistance is vital to our attempts to alleviate the enormous burden of suffering caused by obstructive lung diseases.

Airway patency matters

To the Editor, In their review of preoxygenation, Tanoubi et al. calculated that a preoxygenated adult patient has a pulmonary oxygen reserve that would last nine minutes should the patient become apneic. They base this calculation on estimates of available pulmonary oxygen reserves and oxygen consumption. Although the calculation is theoretically attractive because it illustrates the difference in oxygen reserves in non-preoxygenated and preoxygenated patients, we would argue that the calculation has little clinical relevance. What really matters under those circumstances is whether or not the upper airway is open. The principles of apneic oxygenation (well described 50 years ago) apply in a patient with an open airway. As long as oxygen is flushing over the airway, desaturation might not occur for 50 min or longer. Unfortunately, the nine-minute calculation is also misleading when the upper airway is not open, because the fact that oxygen causes resorption atelectasis is not taken into account. Functional residual capacity will decrease in a healthy adult patient by about 200 mL during the first minute after airway occlusion. Pulmonary shunting can then cause more rapid desaturation, even in patients who are well preoxygenated. Therefore, to take advantage of the principles of apneic oxygenation, it is important to maintain an open airway during induction and to retain an open airway during apnea while oxygen is dispersed over the patient’s face. Although Tanoubi et al. gave an otherwise good review of an interesting subject, we feel that clarifying these issues would have improved their article. Funding The authors have had no funding for the present work and have no association with any individuals or organization that could constitute a conflict of interest in relation to this submission.

Increased load on the respiratory muscles in obstructive sleep apnea

We wished to quantify, in patients with obstructive sleep apnoea (OSA), the activity of the respiratory muscles in relation to upper airway occlusion and patency in sleep. We hypothesized that particular levels of neuromuscular activation are directly associated with upper airway patency. 21 patients with previously diagnosed OSA and 21 healthy control subjects underwent respiratory muscle testing and polysomnography. Neural respiratory drive, as measured by the electromyogram of the diaphragm (EMG(di)) was elevated in the obese OSA patients, awake and supine (13.1(5.6)%max), compared to normal subjects (mean (SD) 8.1(2.3)%max, p<0.01). During unobstructed breathing in sleep (stage N2) normal subjects had an EMG(di) of 7.7(3.9) compared to 22.8(19.2)%max in the OSA group (p<0.001). Prior to airway occlusion, EMG(submandibular) and EMG(di) dropped markedly, and then, following occlusion, increased progressively to their highest levels at airflow onset. Patients with OSA require specific and increased levels of neural respiratory drive to sustain ventilation in sleep.

Electrical stimulation of the hypoglossal nerve in the treatment of obstructive sleep apnea

Upper airway occlusion in obstructive sleep apnea has been attributed to a decline in pharyngeal neuromuscular activity occurring in a structurally narrowed airway. Surgical treatment focuses on the correction of anatomic abnormalities, but there is a potential role for activation of the upper airway musculature, especially with stimulation of the hypoglossal nerve and genioglossus muscle. We present evidence from research on upper airway neuromuscular electrical stimulation in animals and humans. We also present results from eight obstructive sleep apnea patients with a fully implanted system for hypoglossal nerve stimulation, demonstrating an improvement in upper airway collapsibility and obstructive sleep apnea severity. Future research, including optimization of device features and stimulation parameters as well as patient selection, is necessary to make hypoglossal nerve stimulation a viable alternative to positive airway pressure therapy and upper airway surgical procedures.

Oral appliances for the treatment of obstructive sleep apnea

Background: Obstructive sleep apnea (OSA) is a disabling condition which reduces the sufferer’s ability to work effectively due to somnolence during the day. It can be life threatening, resulting in nocturnal anoxia and cardiac arrythmias. OSA is due to intermittent cessation of airflow at the upper airway level of at least 10 seconds duration. Severe cases may stop breathing for 2-3 minutes. It is a rare condition with a prevalence of up to 4 percent in middle aged adults. OSA can be due to central apnea where the neural drive is transiently abolished. In obstructive apnea, the neural drive remains but there is occlusion of the oropharyngieal airway. Therapeutic approaches range from weight reduction, improving nasal patency, avoidance of alcohol and sleeping in the supine position and may include surgical procedures to increase the airway space. Continuous positive airway pressure (CPAP) at night is a common therapeutic modality but not always tolerated by the patient. Objective: This essay reviews current practices using airway dilators. Keywords: Oral airway, sleep apnea, snoring, treatment by oral appliance.

Impact of endotracheal tube size on preextubation respiratory variables

Purpose Many parameters have been evaluated to predict successful extubation. These are all affected by extrapulmonary variables. The purpose of this study was to evaluate the effect of endotracheal tube (ETT) size on preextubation predictors of successful extubation. Materials and Methods Twenty-two intubated and mechanically ventilated subjects were recruited when ready for extubation. Subjects were ventilated with T-piece, continuous positive airway pressure (CPAP) of 5 cm H 2O, and pressure support ventilation (PSV) of 5 cm H 2O in randomized order for 15 minutes each. Pulmonary mechanics—including respiratory frequency ( f), tidal volume ( V T), f/ V T ratio, negative change in esophageal pressure, pressure time product (PTP), work of breathing, and the airway occlusion pressure 100 milliseconds after the onset of inspiratory flow—were measured using a microprocessor-based monitor at the end of each interval. After extubation, measurement of pulmonary mechanics was repeated at 15 and 60 minutes. Results In patients with 7.0- or 7.5-mm ETT compared with patients with 8.0-mm ETT, (1) f was significantly higher during all ventilatory modes and 15 minutes after extubation; (2) V T during PSV and CPAP was significantly lower; (3) mean f/ V T was significantly higher (122 ± 57 vs 69 ± 35, P = .026); and (4) PTP was significantly higher during CPAP, PSV, and 15 minutes after extubation. There was a nonsignificant trend toward increased negative change in esophageal pressure, work of breathing, and airway occlusion pressure 100 milliseconds after the onset of inspiratory flow in the smaller-ETT group. Conclusions The ETT size has a significant impact on f, V T, f/ V T ratio, and PTP.

Obstructive sleep apnea and cardiac arrhythmias

Sleep-disordered breathing (SDB), which includes obstructive sleep apnea (OSA) as its most extreme variant, is characterized by intermittent episodes of partial or complete obstruction of the upper airway, leading to cessation of breathing while asleep. Cardiac arrhythmias are common problems in OSA patients, although the true prevalence and clinical relevance of cardiac arrhythmias remains to be determined. The presence and complexity of tachyarrhythmias and bradyarrhythmias may influence morbidity, mortality and quality of life for patients with OSA. Although the exact mechanisms underlying the link between OSA and cardiac arrhythmias are not well established, they could be some of the same proposed mechanisms relating OSA to different cardiovascular diseases, such as repetitive pharyngeal collapse during sleep, which leads to markedly reduced or absent airflow, followed by oxyhemoglobin desaturation, persistent inspiratory efforts against an occluded airway and termination by arousal from sleep. These mechanisms elicit a variety of autonomic, hemodynamic, humoral and neuroendocrine responses that evoke acute and chronic changes in cardiovascular function. However, despite substantial research effort, the goals of determining in advance which patients will respond most favorably to certain treatment options (such as continuous positive airway pressure, tracheostomy or cardioversion) and the developing alternative treatments remain largely elusive. Therefore, this literature review aims to summarize a broad array of the pathophysiological mechanisms underlying the relationship between OSA and cardiac arrhythmias and the extent of this association from an epidemiological perspective, thereby attempting to assess the effects of OSA treatment on the presence of cardiac arrhythmias.

Severe lingual tonsillar hypertrophy and the rationale supporting early use of wire-guided retrograde intubation

An expanding body of literature exists which describes the airway challenges and management options for lingual tonsillar hypertrophy (LTH). The use of retrograde intubation to secure a patient‘s airway in the setting of LTH has been previously unreported and should be considered early in the event of a cannot intubate, cannot ventilate scenario. A 55-year-old man, who had previously been described as an easy intubation, presented an unexpected cannot intubate, cannot ventilate scenario secondary to LTH. Various noninvasive airway maneuvers were attempted to restore ventilation without success. We describe the advantages of early use of wire-guided retrograde intubation as an alternative to a surgical airway for obtaining a secure airway in a patient with LTH, in whom noninvasive airway management maneuvers have failed. Multiple different noninvasive approaches to management of LTH have been previously described including the laryngeal tube, laryngeal mask airway, and fiberoptic bronchoscopy. Unfortunately, none of these noninvasive airway maneuvers successfully ventilated this patient and an invasive airway became necessary. Retrograde intubation is a less invasive alternative to the surgical airway with potentially less risk for complications. Retrograde intubation may be particularly effective in the setting of LTH as it may stent open an otherwise occluded airway and allow passage of an endotracheal tube. Skillful use of this technique should be considered early as a viable option in any case of unexpected difficult intubation due to LTH.