Dyspnea

Dyspnea is a subjective experience of breathing discomfort that is comprised of qualitatively distinct sensations that vary in intensity. The experience derives from interactions among multiple physiologic, psychologic, social, and environmental factors, and it may induce secondary physiologic and behavioral responses. It is often described as breathlessness, air hunger, shortness of breath, increased work of breathing, chest tightness, and preoccupation with breathing.¹ Dyspnea may be the result of pulmonary disease or many other conditions, such as pain, heart disease, trauma, and anxiety.

The severity of the experience of dyspnea may not directly correlate with the severity of underlying disease.2,3 Either diffuse or focal disturbances of ventilation, gas exchange, or ventilation-perfusion relationships can cause dyspnea, as can increased work of breathing or diseases that damage lung tissue (lung parenchyma). One proposed mechanism involves an impaired sense of effort where the perceived work of breathing is greater than the actual motor response generated. Stimulation of many receptors can contribute to the sensation of dyspnea including mechanoreceptors (the stretch receptors, irritant receptors, and J-receptors), upper airway receptors, and central and peripheral chemoreceptors that interact with the sensory and motor cortex.^4,5

The more severe signs of dyspnea include flaring of the nostrils, use of accessory muscles of respiration, and retraction (pulling back) of the intercostal spaces. In dyspnea caused by parenchymal disease (e.g., pneumonia), retractions of tissue between the ribs (subcostal and intercostal retractions) are observed more often than supercostal retractions (retractions of tissues above the ribs), which predominate in upper airway obstruction. Retractions of any type are more commonly seen in children or in adults who are thin and have poorly developed thoracic musculature. Dyspnea can be quantified by the use of ordinal rating scales or visual analog scales.³

Dyspnea can occur transiently or can become chronic. The first episode commonly occurs with exercise and is called dyspnea on exertion. Orthopnea is dyspnea that occurs when an individual lies flat and is common in individuals with heart failure. The recumbent position redistributes body water, causes the abdominal contents to exert pressure on the diaphragm, and decreases the efficiency of the respiratory muscles. Sitting in a forward-leaning posture or supporting the upper body on several pillows generally relieves orthopnea. Paroxysmal nocturnal dyspnea (PND) occurs when individuals with heart failure or lung disease wake up at night gasping for air and must sit up or stand to relieve the dyspnea.

Cough

Cough is a protective reflex that helps clear the airways by an explosive expiration. Inhaled particles, accumulated mucus, inflammation, or the presence of a foreign body initiates the cough reflex by stimulating irritant receptors in the airway. There are few such receptors in the most distal bronchi and the alveoli; thus it is possible for significant amounts of secretions to accumulate in the distal respiratory tree without cough being initiated. The cough reflex consists of inspiration, closure of the glottis and vocal cords, contraction of the expiratory muscles, and reopening of the glottis, causing a sudden, forceful expiration that removes the offending matter. The effectiveness of the cough depends on the depth of the inspiration and the degree to which the airways narrow, increasing the velocity of expiratory gas flow. Stimulation of cough receptors is transmitted centrally through the vagus nerve, and central modulation of the cough reflex can be influenced by opiates and serotonergic agents.6,7 Cough occurs frequently in healthy individuals; however, those with an inability to cough effectively are at greater risk for pneumonia.

Acute cough is cough that resolves within 2 to 3 weeks of the onset of illness or resolves with treatment of the underlying condition. It is most commonly the result of upper respiratory tract infections, allergic rhinitis, acute bronchitis, pneumonia, congestive heart failure, pulmonary embolus, or aspiration. Chronic cough is defined as cough that has persisted for more than 3 weeks, although some researchers have suggested that 7 or 8 weeks is a more appropriate timeframe because acute cough and bronchial hyperreactivity can be prolonged in some cases of viral infection. In nonsmokers, chronic cough is commonly caused by postnasal drainage syndrome, nonasthmatic eosinophilic bronchitis, asthma, gastroesophageal reflux disease, or heightened cough reflex sensitivity.⁸ In smokers, chronic bronchitis is the most common cause of chronic cough, although lung cancer must always be considered. Individuals taking angiotensin-converting enzyme inhibitors for hypertension may develop chronic cough that resolves with discontinuation of the drug.

Abnormal Sputum

Changes in the amount, consistency, color, and odor of sputum provide information about progression of disease and effectiveness of therapy. The gross and microscopic appearances of sputum enable the clinician to identify cellular debris or microorganisms that aid in diagnosis and choice of therapy.

Hemoptysis is the coughing up of blood or bloody secretions. This is sometimes confused with hematemesis, which is the vomiting of blood. Blood that is coughed up is usually bright red, has an alkaline pH, and is mixed with frothy sputum. Blood that is vomited is dark, has an acidic pH, and is mixed with food particles.

Hemoptysis usually indicates infection or inflammation that damages the bronchi (bronchitis, bronchiectasis) or the lung parenchyma (pneumonia, tuberculosis, lung abscess). Other causes include cancer and pulmonary infarction. The amount and duration of bleeding provide important clues about its source. Bronchoscopy, combined with chest computed tomography (CT), is used to confirm the site of bleeding.⁹

Abnormal Breathing Patterns

Normal breathing (eupnea) is rhythmic and effortless. Ventilatory rate is 8 to 16 breaths per minute, and tidal volume ranges from 400 to 800 ml. A short expiratory pause occurs with each breath, and the individual takes an occasional deeper breath or sigh. Sigh breaths, which help maintain normal lung function, are usually 1.5 to 2 times the normal tidal volume and occur approximately 10 to 12 times per hour.

The rate, depth, regularity, and effort of breathing undergo characteristic alterations in response to physiologic and pathophysiologic conditions. Patterns of breathing automatically adjust to minimize the work of respiratory muscles. Strenuous exercise or metabolic acidosis induces Kussmaul respirations (hyperpnea). Kussmaul respirations are characterized by a slightly increased ventilatory rate, very large tidal volume, and no expiratory pause.

Labored breathing occurs whenever there is an increased work of breathing, especially if the airways are obstructed, as in chronic obstructive pulmonary disease (COPD). If the large airways are obstructed, a slow ventilatory rate, increased effort, prolonged inspiration or expiration, and stridor (high-pitched sounds made during inspiration) or audible wheezing (whistling sounds on expiration) are typical. In small airway obstruction, like that seen in asthma and chronic obstructive pulmonary disease, a rapid ventilatory rate, small tidal volume, increased effort, prolonged expiration, and wheezing are often present.

Restricted breathing is commonly caused by disorders such as pulmonary fibrosis that stiffen the lungs or chest wall and decrease compliance. Restricted breathing is characterized by small tidal volumes and rapid ventilatory rate (tachypnea).

Shock and severe cerebral hypoxia (insufficient oxygen in the brain) contribute to gasping respirations that consist of irregular, quick inspirations with an expiratory pause. Anxiety can cause sighing respirations that consist of irregular breathing characterized by frequent, deep sighing inspirations.

Cheyne-Stokes respirations are characterized by alternating periods of deep and shallow breathing. Apnea lasting 15 to 60 seconds is followed by ventilations that increase in volume until a peak is reached, after which ventilation (tidal volume) decreases again to apnea. Cheyne-Stokes respirations result from any condition that slows the blood flow to the brainstem, which in turn slows impulses sending information to the respiratory centers of the brainstem. Neurologic impairment above the brainstem is also a contributing factor (see Table 17-4 and Figure 17-1).

Hypoventilation and Hyperventilation

Hypoventilation is inadequate alveolar ventilation in relation to metabolic demands. It is caused by alterations in pulmonary mechanics or in the neurologic control of breathing such that minute volume (tidal volume × respiratory rate) is reduced. When alveolar ventilation is normal, carbon dioxide (CO₂) is removed from the lungs at the same rate at which it is produced by cellular metabolism. This maintains arterial CO₂ pressure (Paco₂) at normal levels (40 mmHg). With hypoventilation, CO₂ removal does not keep up with CO₂ production and Paco₂ increases, causing hypercapnia (Paco₂ greater than 44 mmHg). (Table 34-2 contains the definition of gas partial pressure and other pulmonary abbreviations.) This results in an increase in hydrogen ion in the blood, termed respiratory acidosis, which can affect the function of many tissues throughout the body.

Hypoventilation is often overlooked until it is severe because breathing pattern and ventilatory rate may appear normal. Blood gas analysis (i.e., measurement of the Paco₂ of arterial blood) reveals the hypercapnia. Pronounced hypoventilation can cause somnolence or disorientation. In addition, alveolar hypoventilation with hypercapnia results in secondary hypoxemia because the accumulation of alveolar CO₂ displaces oxygen (see Hypercapnia, p. 1251).

Hyperventilation is alveolar ventilation that exceeds metabolic demands. The lungs remove CO₂ at a faster rate than it is produced by cellular metabolism, resulting in decreased Paco₂ or hypocapnia (Paco₂ less than 36 mmHg). Hypocapnia results in a respiratory alkalosis that also can interfere with tissue function. Like hypoventilation, hyperventilation can be determined only by arterial blood gas analysis. Hyperventilation commonly occurs with severe anxiety, acute head injury, and conditions that cause insufficient oxygenation of the blood.

Cyanosis

Cyanosis is a bluish discoloration of the skin and mucous membranes caused by increasing amounts of desaturated or reduced hemoglobin (which is bluish) in the blood. It generally develops when 5 g of hemoglobin is desaturated, regardless of hemoglobin concentration. For example, if total hemoglobin concentration is 15 g/dl of blood, 5 g/dl must be desaturated to cause cyanosis. If total hemoglobin level is 11 g/dl, 5 g/dl must still be desaturated for cyanosis to occur.

Peripheral cyanosis (slow blood circulation in fingers and toes) is most often caused by poor circulation resulting from intense peripheral vasoconstriction, like that seen in Raynaud’s disease, cold environments, or severe stress. Peripheral cyanosis is best seen in the nail beds. Central cyanosis is caused by decreased arterial oxygenation (low Pao₂) from pulmonary diseases or pulmonary or cardiac right-to-left shunts. Central cyanosis is best seen in buccal mucous membranes and lips.

Lack of cyanosis does not necessarily indicate that oxygenation is normal. In adults, cyanosis is not evident until severe hypoxemia is present and, therefore, is an insensitive indication of respiratory failure. For example, severe anemia (inadequate hemoglobin concentration) and carbon monoxide poisoning (in which hemoglobin binds to carbon monoxide instead of binding to oxygen) can result in inadequate oxygenation of tissues without causing cyanosis. Individuals with polycythemia (an abnormal increase in numbers of red blood cells), however, may have cyanosis when tissue oxygenation is adequate. Because polycythemia causes hemoglobin concentration to be greater than normal, 5 g/dl can be desaturated, causing cyanosis, without having much effect on oxygenation. Therefore, the significance of cyanosis as a clinical finding must be interpreted in relation to the underlying pathophysiology. If cyanosis is suggested, the Pao₂ should be measured.

Clubbing

Clubbing is the selective bulbous enlargement of the end (distal segment) of a digit (finger or toe) (Figure 35-1) whose severity can be graded from 1 to 5 based on the extent of nail bed hypertrophy and the amount of changes in the nails themselves. It is usually painless. Clubbing is commonly associated with diseases that interfere with oxygenation, such as bronchiectasis, cystic fibrosis, pulmonary fibrosis, lung abscess, and congenital heart disease. It is rarely reversible with treatment of the underlying pulmonary condition. It can sometimes be seen in individuals with lung cancer even without hypoxemia, because of the effects of inflammatory cytokines and growth factors (hypertrophic osteoarthropathy).¹⁰

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