2: Presentation of the patient with pulmonary disease
OUTLINE
Dyspnea, 18
Cough, 22
Evaluation and Management of Cough, 24
Hemoptysis, 24
Chest Pain, 25
The patient with a pulmonary problem generally comes to the attention of the clinician for one of two reasons: (1) complaint of a symptom that can be traced to a respiratory cause or (2) incidental finding of an abnormality on an imaging study, such as a chest radiograph or computed tomography (CT) scan. Although the former presentation is more common, the latter is not uncommon when a radiograph or CT scan is obtained either for evaluation of a seemingly unrelated problem or as a screening study in a patient at risk for pulmonary disease, such as lung cancer. This chapter focuses on the first case, the patient who comes to the physician with a respiratory-related complaint. In the next and subsequent chapters, frequent references are made to abnormal imaging findings as a clue to the presence of a pulmonary disorder.
Four particularly common symptoms bring the patient with lung disease to the physician: dyspnea (and its variants), cough (with or without sputum production), hemoptysis, and chest pain. Each of these symptoms, to a greater or lesser extent, may result from a nonpulmonary disorder, especially primary cardiac disease. For each symptom, a discussion of some of the important clinical features is followed by the pathophysiologic features and the differential diagnosis.
Dyspnea
Dyspnea, or shortness of breath, is frequently a difficult symptom for the physician to evaluate because it is such a subjective feeling experienced by the patient. It is perhaps best defined as an uncomfortable sensation (or awareness) of one’s own breathing, to which little attention normally is paid. However, the term dyspnea subsumes several sensations that are qualitatively distinct. As a result, when patients are asked to describe in more detail their sensation of breathlessness, their descriptions tend to fall into three primary categories: (1) air hunger or suffocation, (2) increased effort or work of breathing, and (3) chest tightness.
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Not only is the symptom of dyspnea highly subjective and describable in different ways, but the patient’s appreciation of it and its importance to the physician also depend heavily on the stimulus or amount of activity required to precipitate it. The physician must consider how the stimulus, when quantified, compares with the patient’s usual level of activity. For example, a marathon runner who experiences a new symptom of shortness of breath after running 5 miles may warrant more concern than would an elderly man who for many years has had a stable symptom of shortness of breath after walking three blocks. On the other hand, a patient who is limited in exertion by a nonpulmonary problem (e.g., severe arthritis of the hips) may not experience any shortness of breath even in the presence of advanced lung disease. If the person were more active, however, dyspnea would become readily apparent. Such considerations become particularly important when joint replacement or other surgical procedures are being considered to try to improve a given patient’s functional status.
Dyspnea should be distinguished from several other signs or symptoms that may have an entirely different significance. Tachypnea is a rapid respiratory rate (greater than the usual value of 12-20/min). Tachypnea may be present with or without dyspnea, just as dyspnea does not necessarily entail the finding of tachypnea on physical examination. Hyperventilation is ventilation that is greater than the amount required to maintain normal CO2 elimination. Hence, the criterion that defines hyperventilation is a decrease in the PCO2 of arterial blood. Finally, the symptom of exertional fatigue must be distinguished from dyspnea. Fatigue may be due to cardiovascular, neuromuscular, or other nonpulmonary diseases, and the implication of this symptom may be quite different from that of shortness of breath.
Dyspnea is distinct from tachypnea, hyperventilation, and exertional fatigue.
There are some variations on the theme of dyspnea. Orthopnea, or shortness of breath on assuming the recumbent position, is often quantified by the number of pillows or angle of elevation necessary to relieve or prevent the sensation. One of the main causes of orthopnea is an increase in venous return and central intravascular volume on assuming the recumbent position. In patients with cardiac decompensation and either overt or subclinical heart failure, the incremental increase in left atrial and left ventricular filling may result in pulmonary vascular congestion and pulmonary interstitial or alveolar edema. Thus, orthopnea frequently suggests cardiac disease and some element of heart failure. However, orthopnea may be seen in other, non-cardiac disorders. For example, some patients with primary pulmonary disease experience orthopnea, such as individuals with a significant amount of secretions who have more difficulty handling their secretions when they are recumbent. Bilateral diaphragmatic weakness may also cause orthopnea because of greater pressure on the diaphragm by abdominal contents and more difficulty inspiring when the patient is supine rather than upright.
Paroxysmal nocturnal dyspnea is waking from sleep with dyspnea. As with orthopnea, the recumbent position is important, but this symptom differs from orthopnea in that it does not occur immediately or shortly after lying down. Although the implication regarding underlying cardiac decompensation still applies, the increase in central intravascular volume is because of a slow mobilization of tissue fluid, such as peripheral edema, rather than to a rapid redistribution of intravascular volume from peripheral to central vessels. Patients with obstructive sleep apnea also may report awakening during the night with a gasping or choking sensation, but this symptom usually occurs in the context of other features of this condition, such as loud snoring, witnessed apneas during sleep, and excessive daytime somnolence.
Orthopnea, often associated with left ventricular failure, may also accompany some forms of primary pulmonary disease.
Variants that are much more uncommon are only briefly mentioned here. Platypnea is shortness of breath when the patient is in the upright position; it is the opposite of orthopnea. Trepopnea is shortness of breath when the patient lies on either the right side or the left side. The symptom can be relieved by moving to the opposite lateral decubitus position.
Returning to the more general symptom of dyspnea, several mechanisms are proposed rather than a single common thread linking the diverse responsible conditions. In particular, neural output reflecting central nervous system respiratory drive is integrated with input from a variety of mechanical receptors in the chest wall, respiratory muscles, airways, and pulmonary vasculature. If central neural output to the respiratory system is not associated with the expected responses in ventilation and gas exchange, the patient experiences a sensation of dyspnea. Presumably, the relative contributions of each source differ from disease to disease and from patient to patient, and they are responsible for the qualitatively different sensations all included under the term dyspnea. Detailed discussions of the mechanisms of dyspnea can be found in the references at the end of this chapter.
The sensation of dyspnea has a number of underlying pathophysiologic mechanisms.
Studies have attempted to link descriptions of dyspnea with underlying pathophysiologic mechanisms. Although the correlations are not perfect, a patient’s description can sometimes help guide the clinician to the correct diagnosis. Patients who describe their breathlessness as a sense of air hunger or suffocation often have increased respiratory drive, which can be related in part to either a high PCO2 or a low PO2, but this also can occur in the absence of respiratory system or gas exchange abnormalities. The sensation of increased effort or work of breathing is commonly experienced by patients who have high resistance to airflow or abnormally stiff lungs. The sensation of chest tightness, frequently noted by patients with asthma, probably arises from intrathoracic receptors that are stimulated by bronchoconstriction. Because many disorders may produce breathlessness by more than one mechanism (e.g., asthma may have components of all three mechanisms), overlap or a mixture of these different sensations often occurs.
The differential diagnosis includes a broad range of disorders that result in dyspnea (Table 2.1). The disorders can be separated into the major categories of respiratory disease and cardiovascular disease. Dyspnea also may be present in the absence of underlying respiratory or cardiovascular disease in conditions associated with increased respiratory drive, such as pregnancy or hyperthyroidism, or in metabolic disorders, such as mitochondrial myopathies. In addition, dyspnea may be experienced by individuals in several common settings or situations that do not readily fall into the above-mentioned categories, such as patients experiencing panic attacks.
TABLE 2.1
Differential Diagnosis of Dyspnea
Respiratory Disease
Airway disease
Asthma
Chronic obstructive lung disease
Upper airway obstruction
Parenchymal lung disease
Acute respiratory distress syndrome
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Pneumonia
Interstitial lung disease Pulmonary vascular disease
Pulmonary emboli
Pulmonary arterial hypertension Pleural disease
Pneumothorax Pleural effusion “Bellows” disease
Neuromuscular disease (e.g., polymyositis, myasthenia gravis, and Guillain-Barré syndrome) Chest wall disease (e.g., kyphoscoliosis)
Cardiovascular Disease
Elevated pulmonary venous pressure
Left ventricular failure
Mitral stenosis
Decreased cardiac output
Severe anemia
Increased Respiratory Drive
Hyperthyroidism
Pregnancy
Disorders of Oxidative Metabolism
Mitochondrial myopathies
Metabolic myopathies
Other Patient Factors
Deconditioning
Obesity
Anxiety
The first major category consists of disorders at many levels of the respiratory system (airways, pulmonary parenchyma, pulmonary vasculature, pleura, and bellows) that can cause dyspnea. Airway diseases that cause dyspnea result primarily from obstruction to airflow, occurring anywhere from the upper airway to the large, medium, and small intrathoracic bronchi and bronchioles. Upper airway obstruction, which is defined here as obstruction above or including the vocal cords, is caused primarily by foreign bodies, tumors, laryngeal edema (e.g., with anaphylaxis), and stenosis. A clue to upper airway obstruction is the presence of disproportionate difficulty during inspiration and an audible, prolonged,
monophonic gasping sound called inspiratory stridor. The pathophysiology of upper airway obstruction is discussed in Chapter 7.
Airways below the level of the vocal cords, from the trachea down to the small bronchioles, are commonly involved with disorders that produce dyspnea. A localized problem, such as an airway tumor, usually does not by itself cause dyspnea unless it occurs in the trachea or a major bronchus. In contrast, diseases such as asthma and chronic obstructive pulmonary disease are widespread throughout the tracheobronchial tree, with airway narrowing resulting from spasm, edema, secretions, or loss of radial support (see Chapter 4). With this type of obstruction, difficulty with expiration predominates over that with inspiration, and the physical findings associated with obstruction (polyphonic wheezing and prolongation of airflow) are more prominent on expiration.
The category of pulmonary parenchymal disease includes disorders causing inflammation, infiltration, fluid accumulation, or scarring of the alveolar structures. Such disorders may be diffuse in nature, as with the many causes of interstitial or diffuse parenchymal lung disease, or they may be more localized, as occurs with a bacterial pneumonia.
Pulmonary vascular disease results in obstruction or loss of functional blood vessels in the lung. The most common acute type of pulmonary vascular disease is pulmonary embolism, in which one or many pulmonary vessels are occluded by thrombi originating in systemic veins. Chronically, large pulmonary arteries may be blocked by abnormally organized pulmonary emboli, or small pulmonary arteries may be blocked by inflammatory or scarring processes that result in thickening of vessel walls or obliteration of the vascular lumen, ultimately causing pulmonary hypertension.
Two major disorders affecting the pleura may result in dyspnea: pneumothorax (air in the pleural space) and pleural effusion (liquid in the pleural space). With pleural effusions, a substantial amount of fluid must be present in the pleural space to result in dyspnea, unless the patient also has significant underlying cardiopulmonary disease or additional complicating features.
The term bellows is used here for the final category of respiratory-related disorders causing dyspnea. It refers to the pump system that works under the control of a central nervous system generator to expand the lungs and produce airflow. This pump system includes muscles (primarily but not exclusively diaphragm and intercostals) and the chest wall. Primary disease affecting the muscles, their nerve supply, or neuromuscular interaction, including polymyositis, myasthenia gravis, and Guillain-Barré syndrome, may result in dyspnea. Deformity of the chest wall, particularly kyphoscoliosis, produces dyspnea by several pathophysiologic mechanisms, primarily through increased work of breathing. Disorders of the respiratory bellows are discussed in Chapter 19.
The second major category of disorders that produce dyspnea is cardiovascular disease. In the majority of cases, the feature that patients have in common is an elevated hydrostatic pressure in the pulmonary veins and capillaries that leads to a transudation or leakage of fluid into the pulmonary interstitium and alveoli. Left ventricular failure, from either ischemic or valvular heart disease, is the most common example. In addition, mitral stenosis, with increased left atrial pressure, produces elevated pulmonary venous and capillary pressures even though left ventricular function and pressure are normal. A frequent accompaniment of the dyspnea associated with these forms of cardiac disease is orthopnea, paroxysmal nocturnal dyspnea, or both. Although worsening of dyspnea in the supine position is not specific to pulmonary venous hypertension and can also be found in some patients with pulmonary disease, improvement of dyspnea in the supine position is argues against left ventricular failure as the causative factor. Severe anemia is frequently included under cardiac causes of dyspnea because the decreased oxygen content of anemic blood mandates an increased cardiac output to maintain adequate oxygen delivery; dyspnea on exertion may result, depending on the patient’s cardiac reserve.
A third category of conditions associated with dyspnea includes those characterized by increased
respiratory drive but no underlying cardiopulmonary disease. Both thyroid hormone and progesterone
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