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Background: Postoperative pulmonary complications are common. Aging and respiratory disease provoke airway hyperresponsiveness, high-risk surgery induces diaphragmatic dysfunction, and general anesthesia contributes to atelectasis and peripheral airway injury. This study therefore tested the hypothesis that inhalation of penehyclidine, a long-acting muscarinic antagonist, reduces the incidence of pulmonary complications in high-risk patients over the initial 30 postoperative days., Methods: This single-center double-blind trial enrolled 864 patients age over 50 yr who were scheduled for major upper-abdominal or noncardiac thoracic surgery lasting 2 h or more and who had an Assess Respiratory Risk in Surgical Patients in Catalonia score of 45 or higher. The patients were randomly assigned to placebo or prophylactic penehyclidine inhalation from the night before surgery through postoperative day 2 at 12-h intervals. The primary outcome was the incidence of a composite of pulmonary complications within 30 postoperative days, including respiratory infection, respiratory failure, pleural effusion, atelectasis, pneumothorax, bronchospasm, and aspiration pneumonitis., Results: A total of 826 patients (mean age, 64 yr; 63% male) were included in the intention-to-treat analysis. A composite of pulmonary complications was less common in patients assigned to penehyclidine (18.9% [79 of 417]) than those receiving the placebo (26.4% [108 of 409]; relative risk, 0.72; 95% CI, 0.56 to 0.93; P = 0.010; number needed to treat, 13). Bronchospasm was less common in penehyclidine than placebo patients: 1.4% (6 of 417) versus 4.4% (18 of 409; relative risk, 0.327; 95% CI, 0.131 to 0.82; P = 0.011). None of the other individual pulmonary complications differed significantly. Peak airway pressures greater than 40 cm H2O were also less common in patients given penehyclidine: 1.9% (8 of 432) versus 4.9% (21 of 432; relative risk, 0.381; 95% CI, 0.171 to 0.85; P = 0.014). The incidence of other adverse events, including dry mouth and delirium, that were potentially related to penehyclidine inhalation did not differ between the groups., Conclusions: In high-risk patients having major upper-abdominal or noncardiac thoracic surgery, prophylactic penehyclidine inhalation reduced the incidence of pulmonary complications without provoking complications., (Copyright © 2022, the American Society of Anesthesiologists. All Rights Reserved.)

Background: Spontaneous pneumomediastinum most relevant triggering events are cough, vomiting, nutritional problems, physical activity and use of inhaled drugs. Association of spontaneous pneumomediastinum with non-asthma-related bronchospasm is an infrequent event., Clinical Case: This is the case of a 21-year-old woman without personal or family history of asthma, allergic rhinitis or atopy who during late puerperium had 39 °C fever, paroxysmal cough and chest oppression of sudden onset, as well as wheezing and subcutaneous emphysema of the neck; she had no previous nasal symptoms. Chest X-ray revealed free air in the mediastinum and left lateral side of the neck. Possible cause of the condition was attributed to bronchospasm related to airway infection. Treatment was based on bronchodilators, systemic steroids and supplementary oxygen administration. The symptoms subsided after 48 hours., Conclusions: In the clinical case herein presented, spontaneous pneumomediastinum precipitating factor appeared to be paroxysmal cough associated with bronchospasm and, hence, we suggest for this entity to be suspected in patients even if there is no previous history of asthma.

Idiopathic pulmonary hemosiderosis is primarily a disorder of childhood, which is characterized by hemoptysis, iron deficiency anemia, and diffuse parenchymal infiltrates on chest x-ray secondary to recurrent attacks of alveolar hemorrhage. It can be diagnosed by showing hemosiderin laden macrophages in bronchoalveolar lavage fluid after other specific causes of diffuse alveolar hemorrhage are definitely excluded. A 5-year-old male patient was admitted to our clinic with sudden-onset pallor during iron therapy given for anemia. While he was being investigated for clinical and laboratory signs mimicking hemolytic anemia, he developed cough and dyspnea. He had infiltrates on chest x-ray and scattered patchy infiltrates in both lungs on high-resolution computed tomography. Hemosiderin laden macrophages were identified in fasting gastric juice and bronchoalveolar lavage fluid. The patient was diagnosed with idiopathic pulmonary hemosiderosis and started corticosteroid therapy.

Introduction: Idiopathic spontaneous hemothorax has been rarely described in the literature., Case Study: A case of status asthmaticus and spontaneous hemothorax is described in a 29-year-old female of African descent who presented to the emergency room after 2 days of severe cough productive of yellow sputum, otalgia, sore throat, subjective fevers, chills, headache, progressive wheezing, chest tightness and dyspnea. She had a history of 7 years of asthma and was non-adherent with her controller asthma medications. Prophylactic subcutaneous administration of enoxaparin 40 milligrams was initiated upon hospitalization. The patient initially had a normal chest radiograph but subsequently developed a large, left hemothorax that required tube thoracostomy placement followed by video-assisted thoracoscopic surgery (VATS)., Results: The patient was transferred to the Intensive Care Unit (ICU) and tube thoracostomy resulted in evacuation of 1,400 milliliters of blood-like fluid, which had a pleural fluid hematocrit greater than 50% of the serum hematocrit. A contrast-enhanced computed tomography (CT) scan of the chest did not reveal any source for the bleeding and a technetium bone scan of the chest was normal. The patient required transfusion of 5 units of packed red blood cells. She was then taken to the operating room for VATS because of continued chest tube drainage (3,200 milliliters of fluid over a 48-hour period)., Conclusion: The etiology of the hemothorax was unknown despite surgical exploration but was felt to be secondary to cough and bronchospasm associated with status asthmaticus.

Bradykinin has been implicated as a mediator of the acute pathophysiological and inflammatory consequences of respiratory tract infections and in exacerbations of chronic diseases such as asthma. Bradykinin may also be a trigger for the coughing associated with these and other conditions. We have thus set out to evaluate the pharmacology of bradykinin-evoked coughing in guinea pigs. When inhaled, bradykinin induced paroxysmal coughing that was abolished by the bradykinin B2 receptor antagonist HOE 140. These cough responses rapidly desensitized, consistent with reports of B2 receptor desensitization. Bradykinin-evoked cough was potentiated by inhibition of both neutral endopeptidase and angiotensin-converting enzyme (with thiorphan and captopril, respectively), but was largely unaffected by muscarinic or thromboxane receptor blockade (atropine and ICI 192605), cyclooxygenase, or nitric oxide synthase inhibition (meclofenamic acid and N(G)-nitro-L-arginine). Calcium influx studies in bronchopulmonary vagal afferent neurons dissociated from vagal sensory ganglia indicated that the tachykinin-containing C-fibers arising from the jugular ganglia mediate bradykinin-evoked coughing. Also implicating the jugular C-fibers was the observation that simultaneous blockade of neurokinin2 (NK2; SR48968) and NK3 (SR142801 or SB223412) receptors nearly abolished the bradykinin-evoked cough responses. The data suggest that bradykinin induces coughing in guinea pigs by activating B2 receptors on bronchopulmonary C-fibers. We speculate that therapeutics targeting the actions of bradykinin may prove useful in the treatment of cough., (Copyright © 2016 by The American Society for Pharmacology and Experimental Therapeutics.)

Primary Objective: To assess the unusual use of a volatile anaesthetic for treatment of life-threatening bronchospasm in a patient with traumatic brain injury (TBI)., Research Design: Case report., Methods and Procedures: This study presents a previously healthy 30-year-old man with severe TBI and bronchospasm-induced acute hypercapnia. He was treated with inhaled isoflurane in combination with monitoring of intracranial pressure (ICP) and regional cerebral blood flow (rCBF)., Results: Three-day-long isoflurane treatment resolved drug-refractory bronchospasm, decreased airway pressure and improved gas exchange, even at a low end-tidal concentration (0.3-0.5 vol%). Although rCBF was increased by 18 ml min(-1) 100 g(-1) during isoflurane treatment, there was a significant decrease in ICP (21 (SD = 3) mmHg, 9 (SD = 5) mmHg, 2 (SD = 3) mmHg; during pre-treatment, treatment and post-treatment, respectively; p < 0.001). Improved autoregulation due to lower partial pressure of carbon dioxide, restoration of carbon dioxide reactivity, isoflurane-induced regional differences in rCBF and improved microcirculation may have been responsible for the prompt and long-lasting normalization of ICP. The patient had no TBI-related disability at 6 months post-injury., Conclusions: Isoflurane at a low dose can be an effective and safe treatment option for drug-refractory bronchospasm in a patient with traumatic intracranial hypertension, provided that multimodality neuromonitoring is used.

Dyspnoea can be classified into four types with each arising by means of a different mechanism. Air hunger originates from chemoreflex activity. It is inhibited by pulmonary inflation, probably through a reflex induced by stretch receptors in the large airways. The feeling of increased work of breathing particularly occurs during volitional breathing and is augmented by every cause of increased work of breathing or muscle weakness. This feeling is probably induced by activity of the cerebral motor cortex. Tightness of the chest can be due to bronchospasm. This feeling possibly arises from stimulation of 'slowly adapting receptors' in the large airways, which are closely connected to smooth muscle cells. There are indications that tachypnoea can result from the stimulation of pulmonary C fibres. Possible stimuli are pulmonary venous congestion and the intravenous administration of adenosine. Recognizing and understanding the different types of dyspnoea is relevant to the interpretation and treatment of this symptom.

Negative pressure pulmonary edema (NPPE) is an important cause of noncardiogenic pulmonary edema but is rarely reported in the setting of bronchospasm. A 43-year-old woman with severe reactive airway disease suffered an episode of severe bronchospasm after endotracheal extubation following an otherwise uneventful general anesthetic. Subsequently, she developed clinical and radiographic signs of pulmonary edema in the absence of other symptoms of acute left-sided heart failure, leading to the diagnosis of noncardiogenic pulmonary edema. She received noninvasive positive pressure ventilation for a few hours, after which her clinical and radiologic signs and symptoms of pulmonary edema were greatly improved. This clinical scenario strongly suggests NPPE. We submit that it is possible to create NPPE by generating highly negative intrathoracic pressures in the setting of severe bronchospasm.

The successful application of a pumpless extracorporeal lung assist procedure ("interventional lung assist, iLA) in three cases of severe refractory status asthmaticus, which could not be solved with conventional pharmacological and respiratory therapy is reported. After an individual risk-benefit analysis such a therapy can be used to reduce lung injury due to invasive mechanical ventilation. Because of the complexity of this therapy it should only be applied in special medical centers with sufficient experience in dealing with extracorporeal lung assist procedures.

Unlabelled: Spastic bronchitis in infants and young children is one of the most frequent causes of hospitalization in this age group. Both infectious and allergic inflammations lead to inflammation cells activation and their flow to the place of inflammation by the activation of adhesive molecules. One of groups of adhesive molecules are L, E and P selectins responsible for leucocytes migration through the vessel wall. The aim of the study was to assess the concentration of solved fractions of L, P and E selectins in infants and young children in the course of spastic bronchitis., Material and Methods: Fifty four patients with spastic bronchitis (group I) including 32 with the first bronchitis (group IA) and 22 patients with recurrent bronchitis (at last the third one--group IB) were included into the study. Comparative group (group II) was consisted of 26 patients hospitalized due to other causes and with no bronchitis in the past. Patients were from 1 to 36 months of age. Among all patients solved fractions of selectins L, E and P were analyzed by ELISA tests., Results: Mean sL-selectin concentration in group I was 4126.3 ng/ml and in group II 4222.31 ng/ml and was not statistically significant. Concentrations of sL-selectin in the group of patients with the first episode of spastic bronchitis was 4099.37 ng/ml and in the group of patients with recurrent bronchitis was 4166 ng/ml and had no statistical difference. Mean sE-selectin concentration in group I was 205.49 ng/ml and in group II 214.50 ng/ml and was not statistically significant. Concentrations of sE-selectin in the group of patients with the first episode of spastic bronchitis was 195.22 ng/ml and in the group of patients with recurrent bronchitis was 220.43 ng/ml and had no statistical difference. Concentration of sP-selectin was assessed among 51 patients with bronchitis and among 26 patients from comparative group. Because of the lack of normal distribution values of sP-selectin concentrations were changed by decimal logarithm. Mean sP-selectin concentration in group I was 235.95 ng/ml and in group II 164.70 ng/ml. After logarithm change values of concentrations were: 2.249 and 2.005 and had statistical difference (p = 0.0221). Concentrations of sP-selectin in the group of patients with the first episode of spastic bronchitis was 234.0 ng/ml and in the group of patients with recurrent bronchitis was 238.20 ng/ml and after logarithm change concentrations were 2.26 in the group of patients with the first episode of spastic bronchitis and 2.24 in the group of patients with recurrent bronchitis and had no statistical difference., Conclusion: On the ground of our study in infants and young children with spastic bronchitis increase of sP-selectin concentration was observed and sE-selectin and sL-selectin concentrations were the same.

The etiologic role of recently identified respiratory viruses for acute wheezing in children is not yet clear. The purpose of this study was to investigate the prevalence of recently identified viruses, including human metapneumovirus (hMPV), human bocavirus (hBoV), human coronavirus NL63 (hCoV-NL63), and human coronavirus HKU1 (hCoV-HKU1) in children with acute wheezing. Viral etiology was identified in 231 children hospitalized with acute wheezing, aged from 1 month to 5 years. Viral antigens for common respiratory viruses were detected by IFA or multiplex PCR. RT-PCR was used to detect respiratory rhinoviruses, hCoV-NL63, hCoV-HKU1, and hMPV. PCR assays for hBoV DNA were performed using the primer sets for noncapsid protein (NP1) and nonstructural protein (NS1) genes. Viruses were found in 61.5% (142/231) of the study population and a single virus was detected in 45.5% (105/231) of the study population. Rhinovirus (33.3%), human respiratory syncytial virus (hRSV; 13.8%), and hBoV (13.8%) were the most frequently detected viruses. hMPV and hCoV-NL63 were detected in 7.8% and 1.3% of wheezing children, respectively. HCoV-HKU1 was not detected. In 16.0% of the study population, more than one virus was detected. In children with acute wheezing, rhinovirus, hRSV, and hBoV were most frequently detected. Further studies including healthy control subjects are needed to define the clinical significance of hBoV in acute wheezing.

In a 20-year-old woman with known asthma, anaphylactic bronchospasm induced a grave combined respiratory and metabolic acidosis (pH(a) 6.66) with marked hypoxaemia (S(a)O(2) 45%). The beneficial effects of the rightward shift of the oxyhaemoglobin dissociation curve on tissue O(2) unloading at such pH was more than offset by the negative effect on S(a)O(2) at the reduced P(a)O(2) (7.0 kPa) found in this patient. This case illustrates the detrimental effect of grave acidosis on arterial blood oxygen content at subnormal P(a)O(2) values, the beneficial effect of a supranormal P(a)O(2) on the S(a)O(2) in such patients, and the rapid remission rate of life-threatening acidosis and blood lactate after adequate ventilation and tissue oxygenation were secured. The initial treatment of the patient and clinically relevant considerations are discussed.

Unlabelled: Wheezy bronchitis can be the first sign of bronchial asthma thus wheezy bronchitis is under special supervision and its etiologic factors are especially analyzed among infants and young children. Due to diagnostic difficulties in this age group allergic inflammation markers are taken into consideration in aspect of recurrent bronchitis prevention. Such marker is eosinophillic cationic protein (ECP). ECP is released from eosinophilles during the late phase of allergic reaction. The aim of the study was to assess ECP concentrations among infants and young children with wheezy bronchitis., Material and Methods: Ninety-four patients with wheezy bronchitis between 1 month and 36 months old were included into the study (47 with the first episode and 47 with at least third episode). Forty-three patients hospitalized due to other causes, from the same age group (these patients haven't already had any wheezy bronchitis) were included into the control group. Among all patients concentrations of ECP were evaluated (among patients from the study group in the acute phase of the disease) by fluoroimmunoenzymatic method (FEIA) with the use of UniCAP 100 set (Pharmacia & Upjohn Diagnostics AB)., Results: Statistically significant differences of ECP concentrations in blood plasma during wheezy bronchitis among infants and young children in correlation to the control group and higher concentrations were observed among patients with wheezy bronchitis. No statistically significant differences were observed in aspect of ECP concentrations between patients with the first episode and patients with recurrent wheezing. No influence of family history of allergy nor symptoms of allergy were observed whereas higher concentrations of ECP were observed among patients with higher level of CRP CONCLUSION: ECP isn't a good marker of prediction of reccurrent wheezing

Food allergies are more and more numerous, and frequent in children at all ages. At any moment, a clinical manifestation, quickly evolutive and alarming, must need the help call at phone 15, and the intervention of a medical team of SMUR. The departmental, free, cell to 15 for all medical emergencies note a regular increase of these specific calls since ten years, as this following case report shows it.

Background: Sandifer Syndrome is an uncommon clinical entity characterized by gastroesophageal reflux, irritability and abnormal movements of the body and contortions of the neck. The majority of paroxysmal cases, in particular, tend to show an association with epilepsy., Methods: The clinical, laboratory and 6-month observation results of the four patients (two boys, two girls) have been presented., Results: The 6-month prospective observation/treatment of four patients aged between 2 and 14 months (mean age, 6.5 +/- 5.2 months) with a diagnosis of Sandifer Syndrome has been investigated. Due to paroxysmal extensor jerks, two of the patients were misdiagnosed with infantile spasm and they were treated accordingly. In the clinical observations of the patients, abnormal neurobehavioral attacks (irritability, crying, head/eye version, torticollis, extensor spasm and dystonic posture) 5-10 times daily were observed. In two of the patients, motor growth retardation was observed, in one patient, bronchospasm attacks were observed, and in all the patients iron deficiency anemia was observed. The electroencephalograms of the patients which were taken during the routine, sleepless and paroxysmal behaviors were normal; the gastroesophageal scintigraphies were positive in the manner of reflux. Management of the infant with gastroesophageal reflux disease, in addition to nonpharmacological interventions pharmacologic therapy, including metoclopramide HCl and Fe (6 mg/kg per day, oral) was useful for the patients, and their paroxysmal attacks decreased dramatically (0-2 attacks/day)., Conclusion: These findings suggest that infants or children with these atypical movements should be evaluated for Sandifer Syndrome. Expensive and comprehensive neurologic examination may be unnecessary. Early diagnosis permits prompt treatment and relief of the problem. Medical management is usually successful.

Advanced age, smoking habit, obesity or malnutrition, the coexistence of hypercapnia, bronchospasm or bronchial hypersecretion, the lack of pre-operative preparation and/or a prolonged duration of anaesthesia can negatively influence respiratory function in patients undergoing abdominal or thoracic surgery. Spirometric testing of pulmonary function is recommended in patients with a history of tobacco use or dyspnoea who are considered for cardiac or upper abdominal surgery and for all patients who are candidated for lung resection. Spirometry can provide cut-off values of acceptable risk in patients that are candidated for abdominal and thoracic surgery. At-risk patients having resective lung surgery should undergo a split lung function study with quantitative lung scanning or computed tomography in order to estimate the function of residual parenchyma after surgery. In patients with borderline estimated values, a cardiopulmonary exercise test is useful to further stratify surgical risk.(www.actabiomedica.it)

Bronchospasm and airway inflammation can lead to a constellation of irreversible changes in airway structure termed remodeling. Remodeling theory offers insight into the permanent biomechanical and pathologic alterations of asthmatic airways. Structural changes seen in asthmatic patients can include thickening of the airway wall reticular basement membrane (RBM), the presence of an abnormal elastic fiber network, and alterations in airway cartilage structure. Although steroid therapy is helpful in symptomatic control, it does not remedy structural alterations or many aspects of the inflammatory milieu. This article discusses several studies and supports the need for further investigation.

Everyday clinical practice reveals both cases of asthma with non-typical symptoms as well as pseudo-asthmatic syndromes with symptoms typical for asthma. Bronchofiberoscopy is a diagnostic method which may help to overcome many diagnostic problems. Although it is a safe procedure, an increased risk of severe bronchoconstriction exists in patients with asthma. The fear of this complication may cause late diagnosis of some asthma-mimicking diseases and may delay the proper treatment. In the present paper we describe two cases showing the possibility of making diagnostic mistakes, and especially illustrating the role ofbronchoscopy in differential diagnosis of bronchial asthma. The authors remind specific indications for this examination in patients with asthma or those presenting asthma-like symptoms. Safety precautions have been also recollected. If safety rules are met, severe bronchoconstriction in patients with bronchial hyperreactivity can be avoided.

Bronchodilator aerosols are commonly delivered through nebulizers or metered dose inhalers (MDI) to treat bronchospasm. Although the clinical results obtained with both these devices are comparable, the use of MDI offers several advantages like lower drug dose, reduced risk of complications, reliability of dosing, ease of administration, less personnel time and reduced cost. However, in non-intubated, spontaneously breathing patients, the amount of drug inhaled depends on the coordination of the inspiratory phase and delivery of the drug. In severely dyspnoeic or disoriented patients in the casualty department or intensive care settings, this is often not possible. Valved spacers and breath-actuated inhalers may not be easily available in such situations. Also, the spacer devices cannot be connected to the anatomical facemask and the need to discontinue oxygenation for aerosol delivery further limits their use.

Objectives: A five-element lumped pulmonary model was developed to estimate respiratory mechanics automatically and noninvasively. The model was applied to diagnose obstructed endotracheal tube. Events like bronchospasm and stiff chest wall were also tested to determine the specificity of the diagnosis. Cases with positive end-expiratory pressure were also included in the analysis to see the effects of positive end-expiratory pressure on the model., Design: Randomized controlled animal study., Setting: University department of anesthesiology., Subjects: Ten anesthetized, paralyzed, and mechanically ventilated mongrel dogs (19-45 kg) of either gender., Interventions: Two levels of upper airway obstruction were induced in ten dogs by partially constricting the endotracheal tube. Acute bronchial constriction was produced in five dogs by injecting methacholine through a central venous catheter. In the same five dogs, the chest wall was stiffened by wrapping a pressure cuff around the chest. Positive end-expiratory pressure was also applied as a separate event in these five animals., Measurements and Main Results: Airway pressure and flow were continuously recorded at the mouth. Model parameters were iteratively identified until the root mean square error between respiratory impedance (obtained from airway pressure and flow) and model-predicted impedance (calculated using Ohm's law) was minimum. The peak inspiratory pressure increased and the peak expiratory flow rate decreased with increasing levels of partial obstruction. The value of the model parameters R(1) and C(2) increased and C(1) decreased with partial obstructed endotracheal tube, whereas R(1) increased and L and C(2) decreased with bronchospasm. With stiff chest wall, R(2) increased and C(2) decreased. With positive end-expiratory pressure, the L parameter decreased and no significant change in other model parameters was observed. Obstructed endotracheal tube is indicated if R(1) increased > or =30%, C(1) decreased > or =10%, and C(2) increased > or =10% from baseline. The test results using 45 events, including control, three complications, and positive end-expiratory pressure, show that when the model is used to diagnose obstructed endotracheal tube, the method has a sensitivity of 90% and specificity of 97%., Conclusions: During an obstructed endotracheal tube, model parameters change such that the event can be diagnosed noninvasively, automatically, and accurately. The model differentiates between upper airway obstruction and complications like bronchospasm and stiff chest wall.

The effects of equipotent doses of racemic albuterol and levalbuterol on heart rate (HR) in intensive care patients with and without baseline tachycardia were studied. Patients were included if they were hemodynamically stable and required bronchodilator therapy every four hours; patients were excluded if they were maintained on a beta-blocker. Four hours after the most recent bronchodilator treatment, each patient was randomized to receive at least two consecutive doses of albuterol 2.5 mg or levalbuterol 1.25 mg four hours apart via nebulization. HR was recorded at the end of the second dose and 5, 10, 15, 30, 60, 90, 120, 180, and 240 minutes after treatment. Twenty intensive care patients, including 10 with baseline tachycardia and 10 without baseline tachycardia, were enrolled. In patients with baseline tachycardia, the mean largest HR increase was 1.4 beats/min (1.3%) with albuterol and 2.0 beats/min (2.1%) with levalbuterol (both increases were not significant). In patients without baseline tachycardia, the mean largest HR increase was 4.4 beats/min (6.7%) with albuterol (p = 0.04) and 3.6 beats/min (5.0%) with levalbuterol (p = 0.03). Short-term use of nebulized albuterol and levalbuterol was associated with similar changes in HR in intensive care patients with or without baseline tachycardia.

Atherosclerotic coronary artery disease and bronchospastic airway disease frequently coexist in older patients. There are substantial data suggesting reduced mortality with the use of beta-adrenergic blocking drugs in patients with symptomatic coronary artery disease, especially patients who have postmyocardial infarction and/or severe coronary artery disease associated with left ventricular dysfunction. Conversely, the use of beta-adrenergic blocking drugs (even selective beta(1)-adrenergic blocking drugs) has the potential of exacerbating bronchospasm. This prospective registry evaluates the safety of use of selective beta(1)-adrenergic blocking drugs in patients with symptomatic coronary artery disease and bronchospastic airway disease. A total of 835 consecutive patients with symptomatic coronary artery disease were prospectively evaluated for coexisting coronary and bronchospastic airway disease. Of these, 30 patients (mean age: 61 +/- 14 years) met the qualifying inclusion criteria. All these study patients except 1 (29/30 [96%]) reached therapeutic beta-blockade (resting heart rate <70 beats per minute). The 1 patient who discontinued use of beta-adrenergic blocking drugs as a result of lifestyle-limiting bronchospasm had no serious adverse outcome. No hospitalizations were required because of worsening bronchospasm. Ten percent of patients reported increased requirement of inhaled beta(2)-agonist use. The patients were followed for 15 +/- 9 months. One patient died of stroke at 22 weeks of follow-up. In conclusion, use of selective beta(1)-adrenergic blocking drugs at a therapeutic dose is safe (as long as careful clinical follow-up is available) and should be considered in all patients with coexisting symptomatic coronary artery disease and bronchospastic airway disease.

Background: Adenosine cardiac stress is widely used as an alternative to exercise testing during myocardial perfusion imaging (MPI). Dyspnea often accompanies the adenosine stress test. Although known asthmatic patients are excluded from this test because of the danger of bronchospasm, there is incomplete information regarding the role of factors such as chronic obstructive pulmonary disease (COPD) and tobacco smoking in adenosine-induced dyspnea., Patients and Methods: A total of 122 consecutive patients (75 male, 47 female; mean age 59 years, SD 10 years) undergoing pharmacologic stress testing with an intravenous infusion of adenosine also had volume-flow spirometry (Vitalograph Compact, Vitalograph Ltd) before, during, and after the test. The indices assessed were forced expiratory volume in one second, its ratio to the forced vital capacity, and peak expiratory flow rate., Results: Mild to severe symptoms were experienced by 81% of patients during adenosine infusion. More than half the patients had dyspnea, but there was no associated bronchospasm. Although the patients with COPD showed parameters indicative of bronchial resistance compared with those without this problem, there was no further deterioration after adenosine infusion. Similarly, patients with a history of tobacco abuse, despite showing a tendency toward increasing airways resistance, had no bronchospasm during the administration of adenosine., Conclusions: (1) Although dyspnea is a common problem during adenosine stress MPI, it is not associated with any appreciable bronchospasm. (2) COPD and tobacco abuse do not appear to be contraindications to adenosine stress MPI studies. However, it is probably safe to exclude patients with severe COPD from adenosine stress MPI until after further evaluation with larger numbers of patients.

For the early institution of anti-asthma treatment, reliable markers distinguishing the children with asthma from children with virus-associated wheeze are needed. Serum eosinophilic cationic protein (ECP) has been suggested as a marker correlating with the intensity of eosinophilic inflammation. We have studied 27 children (age 3 to 35 months) admitted with acute bronchial obstruction. Each child had been followed for 12 months after the first episode and then assigned to one of two groups (asthma or non-asthma) based on the clinical course. Serum ECP (s-ECP) was taken at the acute episode and again at least 6 months later, when the child was completely symptom-free. Serum ECP was analyzed using the Pharmacia CAP ECP FEIA immunofluorescence system. Mean s-ECP during the acute episode was 26.5 micrograms/L (5.5-69) in the asthma group (n = 14) and 9.7 (5.2-17 micrograms/L) in the non-asthmatics (n = 13), p < 0.01. There was no difference in the s-ECP analyzed during the symptom-free period. Elevated values of serum ECP taken during, but not outside, the acute episodes of bronchial obstruction may be helpful in predicting the development of bronchial asthma in young children with acute obstructive episodes.

VC, FVC, FEV1, FEV1/VC%, PEF, MEF25, MEF50, MEF75 were registered in 24 sarcoidosis patients before and after inhalation of 1 dose of berotec and 1 dose of atrovent. Bronchospasm took place in 20.8% patients. Bronchospasm was the only cause of bronchial obstruction in 16.7%, one of the causes in 4.2%. Contribution of bronchospasm to development of bronchial obstruction was essential in all the examinees (91-100%).

Aim: To clarify the role of bronchospasm in impairment of bronchial permeability in chronic bronchitis., Materials and Methods: Lung capacity (LC), forced lung capacity (FLC), forced expiration volume for 1 second (FEV1), FEV1/LC%, peak volume rate (PVS), maximal volume expiration rate (MVER) at the level of 25, 50 and 75% of LC were measured in 62 patients with chronic obstructive bronchitis before and after inhalation of 1 dose of berotec and 1 dose of atrovent., Results: Bronchospasm was present in 42% of the patients, being the only cause of obstruction in 5% of patients. Other reasons added in 37%. Bronchospasm contribution to obstruction reached 21-40, 41-80, 81-100% in 5, 10 and 27% of patients, respectively., Conclusion: An important role of bronchospasm in development of bronchial obstruction in chronic bronchitis is proved.

Background and Objectives: Local anesthetics in blood absorbed from the epidural space attenuate bronchial hyperreactivity to chemical stimuli. However, it is not documented whether local anesthetics at clinically relevant concentrations improve active wheezing in patients with bronchial asthma., Case Report: We managed a 60-year-old man with bronchial asthma and active wheezing under continuous epidural anesthesia using plain lidocaine. The wheezing gradually diminished 20 minutes after the epidural injection of 13 mL 2% lidocaine and completely disappeared over 155 minutes during continuous epidural injection of 2% lidocaine (6 mL/h). The plasma concentrations of lidocaine in arterial blood during the epidural anesthesia ranged from 2.5 to 3.9 microg/mL. Wheezing reappeared 55 minutes after termination of the continuous epidural injection of lidocaine. The plasma concentration of lidocaine at this time was 1.9 microg/mL., Conclusions: At clinically relevant concentrations, lidocaine in the blood absorbed from the epidural space may improve bronchospasm in patients with bronchial asthma.

An 80-year-old female with bronchospasm associated with lung edema, who had been resistive to conventional medical treatment, was mechanically ventilated with isoflurane in oxygen for 386 hours. A total amount of isoflurane given was 277.6 MAC-hours. A serum inorganic fluoride concentration increased after isoflurane inhalation and it was 26.8 microM when serum urea nitrogen and creatinine were elevated. On the day after discontinuation of isoflurane inhalation, a peak serum inorganic fluoride concentration was 38.9 microM. After discontinuation of isoflurane inhalation, serum urea nitrogen and creatinine decreased and no clinical renal dysfunction was observed. We conclude that this subclinical renal dysfunction was due to antibiotics, advanced age, dehydration and prolonged elevation of serum inorganic fluoride concentration.

The purpose of this study was to investigate whether hypoxic pulmonary vasoconstriction is the major determinant of the computed tomography (CT) pattern of mosaic attenuation in asthmatic patients with induced bronchoconstriction. Thin-section CT was performed at suspended full inspiration immediately and 30 min after methacholine bronchoprovocation in 22 asthmatic subjects, who were randomly assigned to breathe room air (group A, n = 8), oxygen via nasal prongs at 5 l/min (group B, n = 8), and oxygen via face mask at 12 l/min (group C, n = 6). CT changes were quantified in terms of global lung density and density in hypodense and hyperdense areas. Lung parenchymal density increases were greatest in group C and greater in group B than in group A, globally (P = 0.03) and in hypodense regions (P = 0.01). On bivariate analysis, the only change in cross-sectional area was related to change in global density. In hypodense regions, density change was related both to reduction in cross-sectional area (P < 0.0005) and to oxygen administration (P = 0.01). After correction for changes in global lung density, only oxygen was independently related to density increase in hypodense areas (P = 0.02). In induced bronchoconstriction, the CT appearance of mosaic attenuation can be largely ascribed to hypoxic vasoconstriction rather than to changes in lung inflation.

Lung capacity (LC), functional lung capacity (FLC), FEV1, FEV1/LC%, CO25, CO50, CO75 were measured in 56 patients with bronchial asthma in attach-free period before and after inhalation of one-dose berotec and one-dose atrovent. Bronchospasm was registered in 66% of the patients. It was the only cause of bronchial obstruction in 12% of the patients and one of the causes in 54% of them. Contribution of the bronchospasm to development of bronchial obstruction was, as a rule, dominating. This contribution reached 81-100% in 60% of the patients.

The examination of 90 patients suffering from pulmonary tuberculosis with bronchial obstruction (BO) has found bronchospasm in one third of the examinees. In spite of the spasm weakness, its contribution to development of BO is significant: 21-40, 41-80, 81-100% in 4, 6 and 27% of patients.