Pulmonary Hypertension

Pulmonary hypertension (PH) is a spectrum of diseases involving the pulmonary vascular circuit and is defined as an elevation in pulmonary arterial pressures. PH is an uncommon disorder that presents with nonspecific complaints. There remains a significant delay in the diagnosis of PH and initiation of appropriate therapy because often patients are misdiagnosed with more common causes of dyspnea such as obstructive lung diseases like asthma. The diagnosis of PH should be considered in patients who do not fit the usual profile of patients presenting with dyspnea and asthma, especially if they do not respond to therapy. The finding of PH foreshadows a poor outcome if not discovered early and treated aggressively.

Cough

Cough results from forced expulsion, usually against a closed glottis, creating a characteristic sound. It is a natural reflex and defense mechanism that helps the body clear excessive secretions and prevents foreign material from entering the respiratory tract. At times, cough can become excessive, nonproductive, disturbing to the patient, and potentially harmful. Cough is a complex symptom and often requires a multidisciplinary approach to ascertain its cause and effective treatment. Evaluation should be guided by a thorough history and physical examination, and testing should be individualized for cost effectiveness. Habit cough and unexplained cough are diagnoses of exclusion, and any tendency to underdiagnose or overdiagnose these conditions should be avoided. Most over-the-counter cough suppressants are not as effective as previously thought, and their use in routine practice should be minimized. Future research should be conducted to elucidate the mechanisms of cough production and to develop cough-suppressive pharmacotherapy. Allergists, as experts in the management of upper and lower airway disorders, should play a central role in the diagnosis and management of cough.

Obesity and Asthma

The current epidemiologic and experimental evidence for a causal association between obesity and asthma is reviewed in this chapter. Putative mechanisms underlying the association between obesity and asthma, including genetics, changes in lung mechanics and airway smooth muscle physiology, hormonal differences, and detrimental effects of comorbidities and the systemic proinflammatory state of obesity are also discussed. These proposed causal pathways are largely speculative or insufficiently studied. Whereas obesity seems to be closely interrelated with the pathogenesis of asthma in some subjects who have the true “obese asthmatic phenotype,” obesity may simply coexist with asthma in others. Proper identification of subjects with true “obese asthma” may be key to dissecting any causal mechanism. Weight loss is beneficial and should be recommended for obese adults with asthma.

Vocal Cord Dysfunction and Paradoxical Vocal Fold Motion Disorder

Diagnosis of vocal cord dysfunction (VCD) relies on clinical history, inspiratory flow–volume loops, and visualization of vocal cord motion by rhinolaryngoscopy. The treatment of VCD requires a multidisciplinary approach relying on elimination of triggers, treatment of comorbid conditions, and consultation with a speech pathologist. This chapter focuses on VCD as it relates to symptoms that suggest asthma and provides specific information to help with the evaluation of VCD.

Adult Cardiac Conditions

In this chapter, the relationship between asthma and its cardiovascular comorbidities is reviewed. Asthma seems not to be a risk factor for coronary heart disease in middle-aged adults; nevertheless, some reports suggest that subjects with severe asthma, especially females, are at significant risk for ischemic heart disease. Additionally, adult-onset asthma, particularly in females, may be a significant risk factor for coronary heart disease. The physician should know how to differentiate between asthma, chronic obstructive pulmonary disease, and cardiac asthma (congestive heart failure), often a difficult proposition. A systematic evaluation, not only of the presence of comorbid conditions, is necessary to ensure that such comorbidities are adequately treated and controlled so that the effect on asthma is minimized.

Other Pulmonary Abnormalities

The purpose of this chapter is to describe various disorders not described elsewhere in this text that may present as asthma, coexist with asthma, or be confused with asthma. The cardinal symptoms of asthma—cough, wheezing, and dyspnea—are associated with nearly all respiratory illnesses. Because asthma is a common disorder, it is a widespread practice to initially treat the syndrome of cough, wheeze, and dyspnea with bronchodilators or inhaled corticosteroids to determine whether they respond to treatment. When such treatment is unsuccessful or only partially effective, then further evaluation may be necessary, including lung imaging, comprehensive lung function testing, inhalation challenge testing with methacholine or mannitol, and more extensive examination of the upper airway.

Genetic Disorders and Asthma

Primary ciliary dyskinesia, cystic fibrosis, and α‎1-antitrypsin deficiency are autosomal recessive hereditary diseases. These diseases should always be considered in cases of asthma. The diagnosis and management of these diseases, particularly with asthma, is an important challenge for clinicians. However, the diagnosis of these chronic diseases is evolving with better definition of phenotypic features and expansion of diagnostic tests. Optimizing and expanding access to the nongenetic tests is critical for ensuring a timely and accurate diagnosis. Early diagnostic strategies, better understanding of the complex interactions underlying the pathophysiology of lung disease, and emerging treatments show great promise for the future. The discovery of genetic and biomarker studies that will predict individuals at risk to develop the clinical manifestations of these diseases can lead to more personalized treatment strategies and a better prognosis.

Exercise-Induced Bronchoconstriction and Asthma

Exercise-induced bronchoconstriction (EIB) is defined as “the transient narrowing of the airway with increasing airway resistance after exercise.” This chapter, in line with the objective of the book, discusses the relationship between EIB and asthma, with special reference to clinical features, pathophysiologic mechanisms, diagnostic criteria, and treatment preventive options.

Gastroesophageal Reflux

Most asthmatic patients have gastroesophageal reflux (GER), and the evidence is strong that GER plays an important role in some patients with asthma. Despite sophisticated study methods and technologically advanced diagnostic tests, the results of published studies on mechanisms fail to provide a diagnostic test with a degree of certainty great enough to identify which patients have GER-induced or GER-exacerbated asthma and which patients will respond to antireflux therapy. Indeed, even positive results on such direct tests as sputum inspection and scintigraphic monitoring, both of which establish reflux into the tracheobronchial tree, do not necessarily establish cause or effect and cannot be used to predict outcomes. The popular and frequently used ambulatory esophageal pH test (Bravo), believed by many to be the best GER test available, can only suggest, but not prove, the diagnosis of GER-induced asthma, and pH testing cannot be safely relied on to make our clinical decisions. Despite extensive research on mechanisms of GER-induced pulmonary symptoms, we are still forced to fall back on “the therapeutic trial”—a trial of a proton pump inhibitor (PPI) to assess whether asthma improves subjectively and objectively. A good PPI response may not necessarily predict a good surgery response, and a poor response to PPI does not necessarily predict a poor response to antireflux surgery.

Nonallergic Rhinopathies and Lower Airway Syndromes

Nonallergic rhinitis is a heterogeneous disease consisting of wide variety of entities that present with persistent nasal symptoms. “United airways” has become a slogan verging on dogma. The concept gained momentum with the realization that the unifying atopic pathophysiology of the nose and tracheobronchial tree lead to coexistent allergic rhinitis and allergic asthma, respectively. Including nonallergic mechanisms and the differential diagnosis of comorbid rhinitides with reversible and irreversible lower airway obstructive entities is more problematic. Although the nose and foregut-derived tracheobronchial tree have distinct embryonic origins, they share exposure to air, pseudostratified epithelium with extensive submucosal glands, common elements of the innate and acquired mucosal immune systems, and extensive nociceptive and autonomic nervous system sensors and controls. Mechanisms affecting both anatomic sites are likely to develop comorbid disease. Anatomic differences contribute to discrete pathologic conditions, as allowed by the bony box of the nasal cavity versus the cartilaginous walls and elastic alveolar interstitial tethers for bronchi and bronchioles. The diverse pathologic states of the nasal mucosa and their relationships with bronchial hyperresponsiveness are the focus of the remainder of this discussion.