Dyspnea

Chapter 19 Dyspnea



Alex H. Gifford, Donald A. Mahler



What Is Dyspnea?


In healthy people, breathing is an unconscious activity that is regulated by automatic command by groups of neurons in the brain stem to control cyclic contraction and relaxation of the respiratory muscles. With a perturbation of this process, the affected person may experience breathing difficulty or discomfort. This sensation is considered a symptom and typically is referred to as dyspnea, which literally means “disordered breathing” (dys– + –pnea). In 1999, the American Thoracic Society defined dyspnea as “a subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity.” Patients typically cite such discomfort when describing their symptoms: “I am short of breath.” “I can’t get enough air.” “It’s hard to breathe.”


A majority of studies investigating dyspnea have focused on patients with chronic obstructive pulmonary disease (COPD), for two reasons: (1) COPD is the most prevalent respiratory disease, and (2) exertional breathlessness is the major symptom of this condition. Thus, the accumulated knowledge of clinical features of dyspnea and current understanding of the relevant mechanisms and qualities derive in large part from studies involving patients with COPD.


An interesting point is that dyspnea shares many features with pain. Both symptoms are complex neurophysiologic processes that are influenced by physiologic, psychologic, social, and environmental factors. These sensations function as warning signals of potential harm that usually lead the affected individual to reduce activities in order to minimize the complaint and/or to seek medical attention. Like pain, dyspnea can be perceived only by the affected person and has both sensory (how bad is it?) and affective (how does it feel?) components. Because both dyspnea and pain are under behavioral control, any emotional state may worsen these experiences to a degree that may be out of proportion to the magnitude of physiologic impairment. For example, high levels of anxiety and panic attacks are associated with increased breathlessness and more intense pain.


Dyspnea is an important problem in the elderly population, often with a major impact on quality of life. It is estimated that more than 30% of those 65 years of age or older without known cardiorespiratory disease report breathlessness with various activities of daily living, including walking on a level surface or up an incline. An analysis of 124 patients over 70 years of age who were randomly selected from a large family medicine practice revealed that up to 37% had moderate to severe dyspnea, and that dyspnea was associated with poor perceived health, more anxiety and depression, and impaired daily functioning. With any physical activity, including exercise, older people exhibit higher levels of ventilation than those typical for younger persons performing the same amount of physical work. Not clear, however, is whether this increased ventilatory demand in older people is a direct result of the aging process in the respiratory system (secondary to a decrease in lung elasticity, increase in chest wall stiffness, and decrease in respiratory muscle strength) or a consequence of sedentary life style, deconditioning, and possible weight gain, which frequently occur with advancing age in populations of developed countries.


Gender differences in the prevalence and severity of dyspnea among patients with COPD have been documented. For example, women are more likely to report severe dyspnea compared with men despite significantly fewer pack-years of smoking cigarettes and similar frequencies of coughing. In the National Emphysema Treatment Trial involving 1053 patients with severe COPD (emphysema phenotype), women reported greater dyspnea than that described by men when findings were controlled for lung function, age, pack-years of smoking, and proportion of the lung affected by emphysema. Whether this gender difference in dyspnea relates to physiologic differences (compared with men, women have smaller airway lumina, with disproportionately thicker airway walls) is uncertain.



Mechanisms of Dyspnea


The neurophysiologic pathways that mediate the control of breathing (to supply oxygen, to eliminate carbon dioxide, and to maintain acid-base balance) also are relevant to the mechanisms of dyspnea (Figure 19-1). In simple terms, nerve fibers (sensory receptors) send electrical signals (afferent impulses) to the spinal cord, which in turn transmits these signals to the brain.


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Figure 19-1 Neurophysiologic basis of dyspnea. CNS, central nervous system.


The brain interprets these signals as a sensation (dyspnea). Outgoing commands from the brain may then elicit an appropriate response—the affected person may stop the offending activity, for example, or may use a rescue inhaler in an attempt to relieve the breathing difficulty.


Presented next is an overview of the neurophysiology of dyspnea, with details of the important components of the relevant pathways.



Sensory Receptors


Activation of sensory receptors provides afferent information to several brain areas that are perceived as respiratory sensations. Blood gas abnormalities (hypoxemia and hypercapnia), mechanical respiratory loads (increased airway resistance and elastance), disturbances in airway epithelium (e.g., edema, inflammation), and hyperinflation are stimuli that activate sensory receptors. For example, neurons in the carotid bodies (peripheral chemoreceptors) are more sensitive to arterial hypoxemia than are neurons in the aortic bodies, although both contribute to hypoxemic ventilatory responsiveness. Central chemoreceptors located in the ventral medulla respond to changes in bloodstream H+-CO2 equilibrium.


Mechanoreceptors are distributed throughout the lung and the chest wall. Parenchymal stretch receptors transmit information about airway caliber and lung volume to the somatosensory cortex through unmyelinated vagal nerve fibers. C-fibers relay information about airway irritation, which can be demonstrated using various chemical mediators. J-fibers are stimulated by interstitial pressure increases, especially pulmonary edema. The chest wall muscles are innervated by Golgi tendon organs and spindle fibers that project to anterior horn cells of spinal neurons. These structures transduce information on length-tension and spatial relationships to the somatosensory cortex.



Afferent Impulses


Afferent information from sensory receptors are transmitted to brain stem respiratory centers that automatically adjust breathing and also may project to higher brain areas for direct assessment of the status of various stimuli. Well-characterized examples include the following: The glossopharyngeal nerve transmits impulses for peripheral chemoreceptors; the vagus nerve transmits information for rapidly adapting, slowly adapting, and C-fiber lung mechanoreceptors; and cervical spinal nerves 3 to 5 (C3 to C5) transmit sensory information accrued by mechanoreceptors from the diaphragm.


Two different pathways have been proposed to process respiratory sensations to the cerebral cortex. One pathway reflects discriminative processing—that is, awareness of the spatial, temporal, and intensity components (e.g., how bad is it?). With activation of respiratory muscle receptors, afferent information is relayed into the brain stem medulla and is then projected to the ventroposterior thalamus area; from here, projections ascend to the primary and secondary somatosensory cortex. These structures are thought to process the intensity component of dyspnea.


A second pathway reflects affective processing (e.g., how does it feel?). With activation of airway and lung receptors, afferent information is relayed by the vagal nerve to the brain stem medulla and is then projected to the amygdala and medial dorsal areas of the thalamus; from here, projections ascend to the insular and cingulate cortex. These structures are part of the limbic system, which forms the inner border of the cortex and contains rich interconnections among the cerebral cortex, thalamus, and brain stem, and are thought to process the affective component of dyspnea.



Central Nervous System


The central nervous system integrates and processes the sensory information into a combined output carried by the phrenic nerve to the respiratory muscles. Neuroimaging studies demonstrate that the anterior cingulate cortex, amygdala, and thalamus are consistently activated in response to various respiratory perturbations. Activation of cortical neural processes appears to require a gating mechanism that can receive changes in respiratory afferent neural activity and distribute this sensory information to specific cortical areas for cognitive processing. It is believed that the thalamus and hippocampus are critical neural areas for the gating of respiratory sensory input to the cerebral cortex.


The experience of dyspnea is thought to result from a mismatch between incoming afferent information (from one or more activated sensory receptors) and the outgoing central respiratory motor activity.



Neuromodulation by Endogenous Opioids


Endogenous opioids and their receptors are expressed broadly throughout the peripheral and central nervous systems, as well as the respiratory system. Beta-endorphins are one of five groups of naturally occurring opioid peptides that modulate pain and dyspnea. In response to noxious and stressful stimuli, the pituitary gland releases beta-endorphins into the circulation, whereas the brain elaborates endogenous opioids into the cerebrospinal fluid.


Naloxone, an opioid antagonist that readily crosses the blood-brain barrier, has been used to uncover the putative effects of endogenous opioids on modulating dyspnea. Studies using methacholine-induced bronchoconstriction, high-intensity treadmill exercise, and inspiratory resistive breathing (as stimuli to provoke breathlessness) have shown that patients with asthma or COPD report higher ratings of dyspnea after receiving naloxone than after receiving normal saline. These observations support the role of endogenous opioids as neuromodulators of the perception of dyspnea.



The Language of Dyspnea


To help dyspneic patients describe their experience more accurately, questionnaires have been developed that allow for the selection of specific descriptors of breathlessness. It appears that the descriptors selected by patients relate in part to the underlying mechanisms contributing to dyspnea. For example, chest tightness is relatively specific to bronchoconstriction in patients with asthma but is not typically reported by patients with COPD. This perception of tightness presumably is due to activation of sensory receptors located in large airways and can be relieved with use of bronchodilator therapy.


The sense of respiratory work or effort commonly is reported by patients with various conditions including asthma, COPD, interstitial lung disease, and neuromuscular disease. The descriptor “work/effort” of breathing difficulty probably is related to activation of respiratory muscle afferents imposed by mechanical loads (airway narrowing → added resistance; parenchymal edema/infiltrates → added elastance) imposed by certain diseases as well as respiratory muscle weakness. For example, in patients with COPD, the lungs typically hyperinflate during the performance of physical tasks. This dynamic hyperinflation results in two major consequences that contribute to dyspnea: (1) an added elastic load and (2) functional weakening of the diaphragm by shortening of the vertical muscle fibers (Figure 19-2). Although patients with acute asthma initially may experience chest tightness, they typically report that the increased work or effort of breathing develops as airway narrowing progresses as a result of subsequent lung hyperinflation.


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Figure 19-2 Mechanical consequences of dynamic hyperinflation.


A perception of not being able to take in enough air has been described as air hunger, or “unsatisfied inspiration.” This experience is not specific to any particular disease or stimulus. A consistent finding is that patients with various cardiorespiratory conditions generally report greater breathing difficulty during inspiration than with expiration. A clustering of reported sensations such as smothering, suffocating, and air hunger has been documented in patients with panic disorder and idiopathic hyperventilation syndrome who do not have any cardiopulmonary or neuromuscular disease. These findings are consistent with an increase in ventilatory drive.


The three qualities of dyspneic sensations, as described, do not explain all clinical features of breathlessness. Moreover, multiple pathways may combine to contribute to dyspnea in an individual patient. For example, in a patient with cardiogenic pulmonary edema, bilateral pleural effusions, cardiac cachexia, and arterial hypoxemia, dyspnea may be due to activation of carotid body neurons (hypoxemia), stretch receptors (interstitial edema), and Golgi tendon organs and spindle fibers (muscle weakness).



Acute Dyspnea



Initial Evaluation


The rapidity with which dyspnea develops is clinically important. Although a standard definition of acute dyspnea does not exist, potentially life-threatening cardiopulmonary processes often are heralded by unprecedented, severe dyspnea minutes to hours in duration. Whenever possible, details should be sought about the circumstances under which dyspnea began, whether it is associated with other symptoms, and how it has progressed. Knowledge of medications and comorbid conditions also is helpful. Dyspnea in the prehospital environment independently predicts a nearly seven-fold likelihood of hospital admission from the emergency department. Studies have shown that delays in seeking clinical attention for acute exacerbations of asthma, COPD, and congestive heart failure (CHF) are associated with a higher frequency of hospital admissions and worse outcomes.


With any clinical encounter, the focus of the initial assessment is on whether or not the patient is stable (Figure 19-3). If this evaluation reveals evidence of hemodynamic insult or lability, hypotension may need to be treated promptly with intravenous fluids, vasopressors, and/or vasodilators. Airway patency and adequacy may be threatened by a depressed level of consciousness, aspiration, or trauma. Endotracheal intubation may become necessary in such instances and when gas exchange derangements cannot be rectified by supplemental oxygen or noninvasive positive-pressure ventilation. Once these basic support elements are addressed, diagnostic testing can safely proceed.


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Figure 19-3 Initial evaluation of acute dyspnea.



Differential Diagnosis


One approach to the differential diagnosis for acute dyspnea is to consider how processes in certain anatomic regions contribute to this symptom (Table 19-1). Obstruction is the most common mechanism for dyspnea arising from upper airway problems. Stridor, a variably high-pitched, harsh inspiratory noise caused by turbulent airflow, often can be heard in the context of an aspirated foreign body and edema of the epiglottis and laryngeal soft tissues. Prompt evaluation and management of upper airway blockage are critical, because the airway is endangered. Exacerbations of asthma and COPD typically are manifested as bronchospasm, wheeze, and cough. Sputum production is common to exacerbations of COPD associated with acute bronchitis and pneumonia, but its physical characteristics alone are not useful in predicting a causative pathogen. Pleuritic chest pain is sharp, incisive, breath-taking discomfort caused by irritation of the parietal pleural nerve supply along the thoracic cavity. This type of pain can accompany pulmonary embolism, pneumonia with or without pleural effusion, and pneumothorax.



Table 19-1 Differential Diagnosis of Acute Dyspnea

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In an acute coronary syndrome (ACS) or CHF, dyspnea is caused by pulmonary venous hypertension and interstitial fluid accumulation. Sudden dyspnea without chest discomfort is the presenting feature of myocardial infarction in 4% to 14% of events. Papillary muscle rupture with mitral valve incompetence, florid pulmonary edema, and shock complicates myocardial infarction in approximately 7% of affected patients. Neuromuscular diseases more commonly cause chronic, progressive dyspnea, but ventilatory failure can develop over just a few hours in acute idiopathic demyelinating polyneuropathy (AIDP). Dyspnea is a frequent consequence of severe abdominal distention, such as that seen with bowel obstruction. The increased pressure of the abdominal cavity restricts diaphragm excursion, thereby decreasing functional residual capacity. Abdominal pain restricts ventilation as a consequence of muscle splinting, which also can cause atelectasis.



Physical Examination


Inspection of the patient in respiratory distress may be quite revealing. Stigmata of adrenergic excess commonly are present, including hypervigilance, diaphoresis, and tachycardia. The breathing pattern frequently is rapid and shallow, which foreshortens responses to clinical questioning. An exception is the deep and sometimes bradypneic pattern of Kussmaul respirations seen with severe metabolic acidosis, typical of diabetic ketoacidosis. Engagement of accessory inspiratory muscles (e.g., scalenes, intercostals, and sternocleidomastoids) often signals respiratory failure. This finding alone is associated with a nearly three-fold risk of death and a roughly doubled requirement for posthospital care in patients admitted through the emergency department for COPD exacerbation. Among adult asthmatics who were noted to use accessory breathing muscles at the time of hospitalization, percent-predicted FEV1

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Jun 12, 2016 | Posted by in RESPIRATORY | Comments Off on Dyspnea

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