A solitary pulmonary nodule (SPN) is a lesion that is surrounded by pulmonary parenchyma. It is typically ≤30 mm and not associated with additional radiographic features such as hilar adenopathy, atelectasis, or pleural effusion.

Content 2

Content 3

 

 

 

In brief, the algorithm is as follows:

  • If possible, obtain old CT images; 2-year stability usually requires no further follow-up.
  • If no previous images are available, determine whether the SPN is solid or subsolid (subsolid refers to ground-glass nodules through which normal parenchymal structures are visible; these often are slow-growing adenocarcinomas, which require a somewhat different approach).
  • For small solid SPNs (≤8 mm), follow the Fleischner Society guidelines on intervals for repeat CT (Radiology 2005; 237:395).
  • For large solid SPNs (>8 mm), assess the probability of malignancy according to clinical and imaging characteristics (online calculator). Further evaluation depends on whether calculated probability of malignancy is low (<5%), intermediate (5%–60%) or high (>60%) and is based partly on previously published guidelines from the American College of Chest Physicians (Chest 2007; 132:108s).
  • Pure subsolid small SPNs (≤5 mm) require no follow-up; a special algorithm for follow-up imaging is provided for larger subsolid SPNs.

Comment: When I encounter a patient with a solitary pulmonary nodule on CT, I first review the images with a radiologist to ensure the accuracy of the initial reading. If the SPN is ≤8 mm, I follow the Fleischner guidelines; if the SPN is larger, I usually enlist specialist help, unless nodule characteristics (e.g., pattern of calcification) indicate very-low probability of malignancy.

Finally, in the same issue of Chest, researchers describe focus groups in which patients with SPNs related their experiences about what they were told, how they were told, and how they reacted to the news. Communicating with patients about something that "might be cancer . . . we'll follow it" is a tricky business; those of us who discuss SPNs with patients have much to learn from that report.

Reference

The March 2013 issue of Chest includes two reviews on SPNs: One, on radiologic characteristics, includes 16 images that illustrate the spectrum of SPNs; in the other, researchers present a "practical algorithm" for diagnosis and management.

 

 

 

 

 

 

 

 

 

 

 

 

Management and Treatment

 

 

 

 



  • Signs that portend imminent respiratory arrest include:

 

  • Depressed mental status
  • Inability to maintain respiratory effort
  • Cyanosis

 

  • Many patients in respiratory distress often appear anxious and sit bolt upright or in a tripod position. They often breathe rapidly. Stridor or wheezing may be audible. Signs suggestive of severe respiratory distress include:

 

  • Retractions and the use of accessory muscles
  • Brief, fragmented speech
  • Inability to lie supine
  • Profound diaphoresis; dusky skin
  • Agitation or other altered mental status

 

  • A plain chest radiograph and an electrocardiogram are obtained in most emergency department (ED) patients with acute dyspnea. Dyspnea biomarker panels do not appear to improve accuracy beyond clinical assessment and focused testing. The use of ancillary studies in the patient with acute dyspnea is discussed in the text. (See 'Ancillary studies' above.)
  • Three primary goals exist for the emergency clinician faced with an acutely dyspneic patient: optimize arterial oxygenation; determine the need for emergent airway management and ventilatory support; and, establish the most likely causes of dyspnea and initiate treatment. For any patient with acute severe dyspnea, the following measures are performed immediately:

 

  • Oxygen is provided
  • Intravenous access is established and blood obtained for laboratory measurements
  • Cardiac and pulse oximetry monitoring is instituted
  • Airway management equipment is brought to the bedside
  • A screening examination, including an assessment of airway difficulty and a search for rapidly reversible causes (tension pneumothorax, pericardial tamponade, upper airway foreign body) is performed. (See 'Initial interventions and differential diagnosis' above and 'Emergent management' above.)

The clinician must work through a wide differential diagnosis while providing appropriate initial treatment for a potentially life-threatening illness. Airway, breathing, and circulation are the emergency clinician's primary focus when beginning management of the acutely dyspneic patient. Once these are stabilized, further clinical investigation and treatment can proceed.

While there are no symptom-specific data about the prevalence of this problem, the epidemiology of cardiac and pulmonary diseases indicates that the magnitude of the problem is large. Cardiac disease is the leading cause of death in the United States, and individuals with angina or myocardial infarction often experience breathlessness as the major (and sometimes sole) indicator that they are ill [1]. In addition, asthma and chronic obstructive pulmonary disease (COPD) afflict approximately 25 million people in the United States, most of whom seek help from clinicians for relief of breathlessness [2].

Investigations of the language of dyspnea suggest that this symptom represents a number of qualitatively distinct sensations, and that the words utilized by patients to describe their breathing discomfort may provide insights into the underlying pathophysiology of the disease [3-6]. Furthermore, there is a growing recognition that one must distinguish between a "sensation" (the neural activation resulting from the stimulation of a receptor) and a "perception" (the reaction of the individual to that sensation) [7-9]. In addition, for a given intensity of a breathing sensation, the unpleasantness of the sensation may vary with the stimulus [10].

A consensus statement of the American Thoracic Society has defined dyspnea as "a term used to characterize a subjective experience of breathing discomfort that is comprised of qualitatively distinct sensations that vary in intensity. The experience derives from interactions among multiple physiological, psychological, social, and environmental factors, and may induce secondary physiological and behavioral responses" [7].

The respiratory system is designed to maintain homeostasis with respect to gas exchange (adequate oxygenation) and the acid-base status of the organism (adjust PaCO2 to maintain normal pH). Derangements in oxygenation as well as acidemia lead to breathing discomfort. However, the development of dyspnea is a complex phenomenon which, in many patients, is the result of stimulation of a variety of mechanoreceptors throughout the upper airway, lungs, and chest wall, and which must also account for the sensations that arise when there is a mechanical load on the system. The origins of dyspnea associated with the inadequate delivery of oxygen to, or utilization by, peripheral muscles are less well understood, but deserve consideration as well.

The American Thoracic Society (ATS) statement on the mechanisms, assessment, and management of dyspnea, as well as other ATS guidelines, can be accessed through the ATS web site at www.thoracic.org/statements.

The pathophysiology of dyspnea will be reviewed here. Factors affecting the control of ventilation and disorders of ventilation, and an approach to a patient with dyspnea, are presented separately. (See "Control of ventilation" and "Disorders of ventilatory control" and "Approach to the patient with dyspnea".)

INCREASED OUTPUT FROM THE RESPIRATORY CENTERS — Most conditions that are associated with respiratory discomfort are characterized by increases in ventilation in response to derangements in ventilation-perfusion matching, increases in dead space, the presence of metabolic acidosis, or stimulation of pulmonary or chest wall receptors. For many years it was believed that this increase in stimulation of the respiratory centers and the resultant augmentation of activity of the ventilatory muscles was responsible for dyspnea. However, subsequent data suggest that the intensity of respiratory discomfort for a given level of ventilation may vary considerably depending upon the nature of the stimulus giving rise to the hyperpnea, and that stimulation of chemoreceptors can produce dyspnea even in the absence of activation of the respiratory muscles (figure 1).

Chemoreceptors — The peripheral chemoreceptors, located in the carotid bodies and aortic arch, sense changes in the partial pressure of oxygen in arterial blood and are also stimulated by acidosis and hypercapnia. The central chemoreceptors, located in the medulla, respond to changes in pH and PCO2. (See "Control of ventilation".) Acute hypercapnia is generally a much stronger stimulus for respiratory discomfort than is acute hypoxia.

Acute hypercapnia — While acute hypercapnia typically leads to brisk increases in ventilation, dyspnea can result from hypercapnia among ventilator-dependent C1-2 quadriplegics who lack functioning respiratory muscles, and in normal subjects paralyzed with neuromuscular blocking agents [11,12]. In a different experimental model, normal subjects maintaining a targeted ventilation experienced greater dyspnea when made hypercapnic than when eucapnic conditions were maintained [13]. These results are consistent with the notion that there are direct projections from the chemoreceptors to the sensory cortex, ie, there is a "corollary discharge" or neural discharge to the sensory cortex that is generated simultaneously with and in proportion to the brainstem neural output to the respiratory muscles [14].

Acute hypoxemia — Acute hypoxemia is also associated with increases in ventilation and respiratory discomfort. While the data supporting a direct role for hypoxic stimulation of chemoreceptors in the production of dyspnea are less clear than with hypercapnia, it seems likely that hypoxemia can produce breathing discomfort independently of changes in ventilation. As examples:

 

  • Subjects exercising under hypoxic conditions experience more dyspnea than when performing the same activity while breathing room air, and less dyspnea when breathing 100 percent oxygen [15].
  • Similar results have been obtained in patients with COPD who exercise with varying degrees of hypoxia [16].
  • Progressive hypoxemia in normal subjects is associated with greater breathing discomfort than comparable degrees of ventilation resulting from exercise [17], demonstrating an effect of hypoxemia on dyspnea that is independent of minute ventilation.

STIMULATION OF MECHANORECEPTORS — Throughout the airways, lungs, and chest wall are a variety of receptors that assist the body in monitoring changes in pressure, flow, and volume in the respiratory system. Information from these receptors is integrated by the central nervous system in a manner that modulates the intensity of dyspnea. However, in some cases, most notably the "chest tightness" associated with bronchoconstriction, the receptors may be the primary source of the sensation [18,19].

Upper airway receptors — Stimulation of receptors in the face and upper airway, which are largely innervated by the trigeminal nerve, can reduce the intensity of dyspnea. As examples, cold air directed against the face increases breathholding time and reduces the respiratory discomfort associated with breathing against an inspiratory load [20,21]. Presumed stimulation of flow or temperature receptors by the inhalation of cold air reduces exertional dyspnea and ventilation in patients with COPD, while reductions in upper airway receptor stimulation achieved with topical lidocaine or by the inhalation of warm, humidified air worsen respiratory discomfort in normal subjects [22,23].

Pulmonary receptors — The lung is populated by three major categories of receptors that transmit information relevant to respiratory sensation to the central nervous system via the vagus nerve:

 

  • Slowly adapting receptors, also known as pulmonary stretch receptors, are activated by an increase in tension in the walls of airways, thereby providing information about increases in lung volume.
  • Rapidly adapting receptors or irritant receptors are stimulated by rapid changes in lung volume, direct mechanical stimuli, or inhalation of irritant particulate matter or chemicals such as histamine.
  • C-fibers are unmyelinated afferent nerve fibers that originate in J-receptors located in small airways and near alveolar capillaries; they are stimulated by mechanical and chemical factors.

The configuration of these receptors is such that limitations of the movement of the respiratory system exacerbate dyspnea in a variety of experimental conditions, including breathholding and acute hypercapnia [24-26]. Restriction of tidal volume associated with hyperinflation may also contribute to the discomfort experienced by patients with emphysema [27].

Inhaled furosemide is hypothesized to stimulate pulmonary stretch receptors. It has been shown to reduce dyspnea in healthy subjects in whom dyspnea was induced using a large resistive load plus hypercapnia [28]. Similarly, dyspnea associated with acute hypercapnia and a restricted tidal volume, as well as the breathlessness associated with exercise, are ameliorated by inhaled furosemide [29,30].

Stimulation of pulmonary receptors may provoke the dyspnea of asthma. While the work of breathing is increased in patients with acute bronchoconstriction due to changes in airways resistance and hyperinflation, the intensity of dyspnea is greater with acute bronchoconstriction than with external resistive loads at comparable degrees of airway resistance [18,19], and the quality of the discomfort is different [3,4,18,19,31]. Breathing against an external load leads to a sensation of increased "effort" or "work" of breathing, while acute bronchospasm is associated with a sensation of "chest tightness or constriction." Furthermore, the inhalation of lidocaine appears to blunt the dyspnea of bronchoconstriction, consistent with the hypothesis that stimulation of pulmonary receptors is contributing to the breathing discomfort [18]. Activation of pulmonary receptors may also play a role in the dyspnea of acute pulmonary embolism [32].

Chest wall receptors — Information from muscle spindles and tendon organs within the chest wall is also important to the perception of dyspnea. Muscle spindles function as length or stretch receptors, while tendon organs monitor force generation. As noted above, constrained chest wall movement exacerbates dyspnea associated with acute hypercapnia, although the relative roles of pulmonary and chest wall receptors are difficult to ascertain [25,26].

Investigators have studied the importance of chest wall receptors on dyspnea by applying mechanical vibrators to the intercostal space, resulting in stimulation of muscle spindles. In-phase vibration, ie, vibration applied to the inspiratory muscles during inspiration, reduces dyspnea in normal subjects made breathless with hypercapnia and an external resistive load [33]. Similar results were obtained in patients with COPD at rest [34] and while breathing carbon dioxide [35], although vibration appeared to have little effect at higher degrees of discomfort associated with exercise on a cycle ergometer [35]. Timing of the stimulation also appears to be important because out-of-phase vibration, ie, vibration of inspiratory muscles during expiration, heightens the intensity of dyspnea [36]. It is important to note that the vibration used in these studies might also have stimulated pulmonary receptors.

While stimulation of chest wall receptors likely plays a role in the detection of changes in thoracic expansion, pulmonary receptors are sufficient to monitor lung volume. Patients with cervical spinal cord injury, for example, in whom information from chest wall receptors is interrupted before reaching the brain, can detect small changes in tidal volume and experience respiratory discomfort when tidal volumes are reduced [37,38].

MECHANICAL LOADING OF THE RESPIRATORY SYSTEM — A wide variety of cardiopulmonary diseases are associated with an increased mechanical load due to changes in airways resistance or pulmonary or chest wall compliance. To achieve a given tidal volume under these conditions, the brain must generate a greater neural output to the ventilatory muscles.

Outgoing motor commands to the ventilatory muscles probably are associated with a corollary discharge to the sensory cortex, which is perceived as a "sense of effort" [39]. The sense of effort appears to be a function of the ratio of the pressure generated by the ventilatory muscles on a given breath to the maximal pressure achievable by the muscles [40]. Thus, the sense of effort may increase because there is an obstruction to flow and the intrathoracic pressure generated on each breath is high, or because the pressure-generating capacity of the muscles is reduced, as is seen in the presence of muscle fatigue, myopathy, or hyperinflation.

Normal subjects maintaining a constant ventilatory target experience less effort but more dyspnea when hypercapnic than eucapnic [13]. While mechanical loading and the effort to breathe are common features of dyspnea in many disease states, they do not explain respiratory discomfort in all settings.

NEUROMECHANICAL DISSOCIATION — Efferent neural impulses exit the brain and proceed to the ventilatory muscles, where they trigger contraction, generation of negative pressure within the thorax, and inspiratory air flow with expansion of the lungs and chest wall. If there is a mechanical load suddenly imposed on the respiratory system with no change in the neurologic command to the ventilatory muscles, the muscles will not shorten appropriately for the tension being generated, intrathoracic pressures will be less negative than normal, inspiratory flow will be reduced, and tidal volume will be diminished.

Although the exact means by which the body makes the comparison between what is expected under normal conditions for a given efferent message and the actual outcome of that message remains unclear, the mismatch between the two (termed "efferent-reafferent dissociation" [41] or "neuromechanical dissociation" [42]) appears to worsen the intensity of dyspnea. This mechanism may in part explain the dyspnea associated with experimentally constrained ventilation [25,26], hyperinflation in COPD [27,42,43], hyperinflation in asthma [44], and in some patients on mechanical ventilators [45]. It may also explain the amelioration of dyspnea with chest wall vibration [33-35] or a flow of air on the face [21].

In these last two examples, receptors in the chest wall and in the distribution of the trigeminal nerve are stimulated exogenously. It is believed that such stimulation, by conveying to the brain information that would indicate the respiratory system had achieved greater flows or volume displacement than actually had occurred, would lead to reduced discrepancy between the efferent neural command and the "apparent" mechanical response, thereby diminishing the intensity of dyspnea.

IMPAIRED OXYGEN DELIVERY OR UTILIZATION — Anemia and cardiovascular deconditioning are two common clinical conditions that are associated with exertional dyspnea and do not readily fit into the categories outlined above.

Anemia — Patients with moderate to severe anemia typically experience breathing discomfort with light exercise despite the absence of a gas exchange abnormality or mechanical loading of the respiratory system. The response of the body to the reduced oxygen-carrying capacity of the blood is to increase cardiac output. This may necessitate an increase in left ventricular end-diastolic pressure with consequent increases in pulmonary venous pressures, the development of interstitial edema, and stimulation of C-fibers. However, tachycardia, rather than increased stroke volume, is often the first response of the cardiovascular system, and it is unclear to what extent intracardiac and pulmonary vascular pressures rise in this setting.

An alternative explanation is that the reduced delivery of oxygen to the metabolically active muscles may lead to the development of a localized metabolic acidosis and the stimulation of "ergoreceptors" in the peripheral muscles [46,47]. Another possibility is that the ventilatory muscles are impaired by the reduced oxygen delivery, which could lead to muscle fatigue under conditions of sustained hyperpnea.

Deconditioning — An individual's fitness is determined by the ability of the cardiovascular system to deliver oxygenated blood to the muscles and by the capability of the muscles to utilize that oxygen via aerobic metabolism to engage in mechanical work. Exercise programs improve fitness by training the heart to generate a greater cardiac output and by inducing enzyme changes in skeletal muscle to improve the efficiency of oxygen use. (See "Exercise physiology".)

Many patients with chronic lung disease assume a sedentary lifestyle and become deconditioned; functional capabilities may be determined more by their level of fitness than by their underlying respiratory illness [48]. Dyspnea on exertion in these individuals may result primarily from the utilization of anaerobic metabolism at low levels of exercise, development of a metabolic acidosis, and increased neural output from the respiratory centers. Whether the development of localized acidosis and stimulation of ergoreceptors also play a role in this situation remains uncertain.

NEURAL ACTIVATION ASSOCIATED WITH BREATHING DISCOMFORT — Investigators have begun to employ positron emission tomography and magnetic resonance imaging as tools to localize regions of the brain that are activated when breathing discomfort is induced experimentally. Acute hypercapnia [49], restriction of tidal volume [50], and imposition of external resistive loads [51,52] have all led to activation of areas within the limbic system and, to a lesser degree, within the brainstem. These areas of the brain also are likely to be involved in the perception of uncomfortable sensations such as pain and hunger. Whether future studies utilizing this technique will identify clearly delineated neural pathways for different types of dyspnea remains to be seen.

SUMMARY — Breathing discomfort is a complex set of sensations which clinicians group under the term dyspnea. The physiologic mechanisms underlying these sensations are varied, and multiple mechanisms may be present in a given patient (figure 1). The individual with COPD, for example, may experience breathlessness because of hypoxemia (increased neural input from peripheral chemoreceptors and output from the respiratory centers), increased airways resistance and hyperinflation (mechanical loading), and neuromechanical dissociation. In the presence of an acute respiratory infection or volume overload, stimulation of pulmonary receptors may also play a role. Appreciation for the complexity of the system allows one to better understand the changes in symptoms that occur over time in a given patient, and permits a more rational therapeutic program to ameliorate a potentially disabling symptom.

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

  1. Cook DG, Shaper AG. Breathlessness, lung function and the risk of heart attack. Eur Heart J 1988; 9:1215.
  2. Higgins M. Epidemiology of obstructive pulmonary disease. In: Principles and Practice of Pulmonary Rehabilitation, Casaburi R, Petty TL (Eds), WB Saunders, Philadelphia 1993. p.10.
  3. Simon PM, Schwartzstein RM, Weiss JW, et al. Distinguishable types of dyspnea in patients with shortness of breath. Am Rev Respir Dis 1990; 142:1009.
  4. Elliott MW, Adams L, Cockcroft A, et al. The language of breathlessness. Use of verbal descriptors by patients with cardiopulmonary disease. Am Rev Respir Dis 1991; 144:826.
  5. Mahler DA, Harver A, Lentine T, et al. Descriptors of breathlessness in cardiorespiratory diseases. Am J Respir Crit Care Med 1996; 154:1357.
  6. Schwartzstein RM. The language of dyspnea. In: Dyspnea: Mechanisms, measurement, and management, Mahler DA, O'Donnell DE (Eds), Marcel Dekker, New York 2005. p.115.
  7. Dyspnea. Mechanisms, assessment, and management: a consensus statement. American Thoracic Society. Am J Respir Crit Care Med 1999; 159:321.
  8. Scano G, Ambrosino N. Pathophysiology of dyspnea. Lung 2002; 180:131.
  9. Jensen D, Webb KA, Davies GA, O'Donnell DE. Mechanisms of activity-related breathlessness in healthy human pregnancy. Eur J Appl Physiol 2009; 106:253.
  10. Banzett RB, Pedersen SH, Schwartzstein RM, Lansing RW. The affective dimension of laboratory dyspnea: air hunger is more unpleasant than work/effort. Am J Respir Crit Care Med 2008; 177:1384.
  11. Banzett RB, Lansing RW, Reid MB, et al. 'Air hunger' arising from increased PCO2 in mechanically ventilated quadriplegics. Respir Physiol 1989; 76:53.
  12. Banzett RB, Lansing RW, Brown R, et al. 'Air hunger' from increased PCO2 persists after complete neuromuscular block in humans. Respir Physiol 1990; 81:1.
  13. Demediuk BH, Manning H, Lilly J, et al. Dissociation between dyspnea and respiratory effort. Am Rev Respir Dis 1992; 146:1222.
  14. Banzett RB, Lansing RW. Respiratory sensations arising from pulmonary and chemoreceptor afferents. In: Respiratory Sensation, Adams L, Guz A (Eds), Marcel Dekker Inc, New York 1996. p.155.
  15. Chronos N, Adams L, Guz A. Effect of hyperoxia and hypoxia on exercise-induced breathlessness in normal subjects. Clin Sci (Lond) 1988; 74:531.
  16. Lane R, Cockcroft A, Adams L, Guz A. Arterial oxygen saturation and breathlessness in patients with chronic obstructive airways disease. Clin Sci (Lond) 1987; 72:693.
  17. Adams L, Lane R, Shea SA, et al. Breathlessness during different forms of ventilatory stimulation: a study of mechanisms in normal subjects and respiratory patients. Clin Sci (Lond) 1985; 69:663.
  18. Taguchi O, Kikuchi Y, Hida W, et al. Effects of bronchoconstriction and external resistive loading on the sensation of dyspnea. J Appl Physiol 1991; 71:2183.
  19. Moy ML, Woodrow Weiss J, Sparrow D, et al. Quality of dyspnea in bronchoconstriction differs from external resistive loads. Am J Respir Crit Care Med 2000; 162:451.
  20. McBride B, Whitelaw WA. A physiological stimulus to upper airway receptors in humans. J Appl Physiol 1981; 51:1189.
  21. Schwartzstein RM, Lahive K, Pope A, et al. Cold facial stimulation reduces breathlessness induced in normal subjects. Am Rev Respir Dis 1987; 136:58.
  22. Spence DP, Graham DR, Ahmed J, et al. Does cold air affect exercise capacity and dyspnea in stable chronic obstructive pulmonary disease? Chest 1993; 103:693.
  23. Simon PM, Basner RC, Weinberger SE, et al. Oral mucosal stimulation modulates intensity of breathlessness induced in normal subjects. Am Rev Respir Dis 1991; 144:419.
  24. FOWLER WS. Breaking point of breath-holding. J Appl Physiol 1954; 6:539.
  25. Chonan T, Mulholland MB, Cherniack NS, Altose MD. Effects of voluntary constraining of thoracic displacement during hypercapnia. J Appl Physiol 1987; 63:1822.
  26. Schwartzstein RM, Simon PM, Weiss JW, et al. Breathlessness induced by dissociation between ventilation and chemical drive. Am Rev Respir Dis 1989; 139:1231.
  27. O'Donnell DE, Bertley JC, Chau LK, Webb KA. Qualitative aspects of exertional breathlessness in chronic airflow limitation: pathophysiologic mechanisms. Am J Respir Crit Care Med 1997; 155:109.
  28. Nishino T, Ide T, Sudo T, Sato J. Inhaled furosemide greatly alleviates the sensation of experimentally induced dyspnea. Am J Respir Crit Care Med 2000; 161:1963.
  29. Moosavi SH, Binks AP, Lansing RW, et al. Effect of inhaled furosemide on air hunger induced in healthy humans. Respir Physiol Neurobiol 2007; 156:1.
  30. Jensen D, Amjadi K, Harris-McAllister V, et al. Mechanisms of dyspnoea relief and improved exercise endurance after furosemide inhalation in COPD. Thorax 2008; 63:606.
  31. Simon PM, Schwartzstein RM, Weiss JW, et al. Distinguishable sensations of breathlessness induced in normal volunteers. Am Rev Respir Dis 1989; 140:1021.
  32. Manning HL, Schwartzstein RM. Pathophysiology of dyspnea. N Engl J Med 1995; 333:1547.
  33. Manning HL, Basner R, Ringler J, et al. Effect of chest wall vibration on breathlessness in normal subjects. J Appl Physiol 1991; 71:175.
  34. Sibuya M, Yamada M, Kanamaru A, et al. Effect of chest wall vibration on dyspnea in patients with chronic respiratory disease. Am J Respir Crit Care Med 1994; 149:1235.
  35. Cristiano LM, Schwartzstein RM. Effect of chest wall vibration on dyspnea during hypercapnia and exercise in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1997; 155:1552.
  36. Homma I, Obata T, Sibuya M, Uchida M. Gate mechanism in breathlessness caused by chest wall vibration in humans. J Appl Physiol 1984; 56:8.
  37. Banzett RB, Lansing RW, Brown R. High-level quadriplegics perceive lung volume change. J Appl Physiol 1987; 62:567.
  38. Manning HL, Shea SA, Schwartzstein RM, et al. Reduced tidal volume increases 'air hunger' at fixed PCO2 in ventilated quadriplegics. Respir Physiol 1992; 90:19.
  39. McCloskey DI. Corollary discharges: Motor commands and perception. In: Handbook of Physiology, Section I, The Nervous System, Brookahrt JM, Mountcastle VB (Eds), American Physiological Society, Bethesda 1981. Vol II, p.1415.
  40. Killian KJ, Gandevia SC, Summers E, Campbell EJ. Effect of increased lung volume on perception of breathlessness, effort, and tension. J Appl Physiol 1984; 57:686.
  41. Schwartzstein RM, Manning HL, Weiss JW, Weinberger SE. Dyspnea: a sensory experience. Lung 1990; 168:185.
  42. O'Donnell DE, Webb KA. Exertional breathlessness in patients with chronic airflow limitation. The role of lung hyperinflation. Am Rev Respir Dis 1993; 148:1351.
  43. O'Donnell DE, Banzett RB, Carrieri-Kohlman V, et al. Pathophysiology of dyspnea in chronic obstructive pulmonary disease: a roundtable. Proc Am Thorac Soc 2007; 4:145.
  44. Lougheed MD, Fisher T, O'Donnell DE. Dynamic hyperinflation during bronchoconstriction in asthma: implications for symptom perception. Chest 2006; 130:1072.
  45. Manning HL, Molinary EJ, Leiter JC. Effect of inspiratory flow rate on respiratory sensation and pattern of breathing. Am J Respir Crit Care Med 1995; 151:751.
  46. Clark AL, Piepoli M, Coats AJ. Skeletal muscle and the control of ventilation on exercise: evidence for metabolic receptors. Eur J Clin Invest 1995; 25:299.
  47. Clark A, Volterrani M, Swan JW, et al. Leg blood flow, metabolism and exercise capacity in chronic stable heart failure. Int J Cardiol 1996; 55:127.
  48. Killian KJ, Leblanc P, Martin DH, et al. Exercise capacity and ventilatory, circulatory, and symptom limitation in patients with chronic airflow limitation. Am Rev Respir Dis 1992; 146:935.
  49. Corfield DR, Fink GR, Ramsay SC, et al. Evidence for limbic system activation during CO2-stimulated breathing in man. J Physiol 1995; 488 ( Pt 1):77.
  50. Banzett RB, Mulnier HE, Murphy K, et al. Breathlessness in humans activates insular cortex. Neuroreport 2000; 11:2117.
  51. Peiffer C, Poline JB, Thivard L, et al. Neural substrates for the perception of acutely induced dyspnea. Am J Respir Crit Care Med 2001; 163:951.
  52. von Leupoldt A, Sommer T, Kegat S, et al. Down-regulation of insular cortex responses to dyspnea and pain in asthma. Am J Respir Crit Care Med 2009; 180:232

 

--------------------------------------------------------------------------

Immediate Management

Oxygen Mask

Intubation

Blood Gases

 

 

 

 

Pediatric

Work Up: Adults

Acute
  • Tab 2
Content 1
Content 2
Chronic
Content 2

 

 

  • Bronchitis
  • Tab 2

Abstract;An estimated 80% to 90% of the risk of developing COPD is accounted for by smoking. In Japan, the Nippon COPD Epidemiology (NICE) study showed that the prevalence of COPD was 8.5%, with incidence of COPD 12.3% among smokers and 4.7% among nonsmokers. As cigarette smokers increased in Japan after 1960, the risk of death due to COPD has increased about 20 years later. In the pathogenesis of COPD, noxious particles and gases inhaled during tobacco smoking cause lung inflammation, induce tissue destruction, impair the defense mechanisms, and disrupt the repair mechanisms.1 These changes lead to COPD. Cigarette smoke activates macrophages and epithelial cells to produce TNF-.ALPHA. and also causes macrophages to release other inflammatory mediators, including the neutrophil chemoattractants IL-8 and LTB 4. In addition to inflammation, processes thought to be important in the pathogenesis of COPD are an imbalance of proteinases and antiproteinases, and oxidative stress. 

Link: Treatment

Reference

1. http://sciencelinks.jp/j-east/article/200522/000020052205A0884619.php

Content 2

 

Breathlessness and labored breathing are common in people with chronic diseases, such as advanced diabetes, cancer, cystic fibrosis, HIV-AIDS, heart disease, COPD, bronchitis, and many other conditions. It can appear on exertion, after meals, during night sleep, or at pregnancy.

 

This Section is:

Authored by xxxxx, MD, last current edit:

Reviewed by xxxx, MD last current review: