Dyspnea

From Wikipedia, the free encyclopedia
  (Redirected from Dyspnoea)
Jump to: navigation, search
Dyspnea
ICD-10 R06.0
ICD-9 786.09
DiseasesDB 15892
MedlinePlus 003075
MeSH D004417

Dyspnea (/dɪspˈnə/ disp-NEE; also dyspnoea; Latin: dyspnoea; Greek: δύσπνοια, dýspnoia), shortness of breath (SOB), or air hunger,[1] is the subjective symptom of breathlessness.[2][3]

The clinical definition of dyspnea is an uncomfortable awareness of one's breathing effort. It is a normal symptom of heavy exertion but becomes pathological if it occurs in unexpected situations.[2] In 85% of cases it is due to either asthma, pneumonia, cardiac ischemia, interstitial lung disease, congestive heart failure, chronic obstructive pulmonary disease, or psychogenic causes.[4] Treatment typically depends on the underlying cause.[5]

Definition[edit]

The American Thoracic Society defines dyspnea as: "A subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity."[6] Other definitions describe it as "difficulty in breathing",[7] "disordered or inadequate breathing",[8] "uncomfortable awareness of breathing",[3] and as the experience of "breathlessness" (which may be either acute or chronic).[2][5][9]

Dyspnea is distinct from labored breathing, which is a common physical presentation of respiratory distress.[citation needed]

Differential diagnosis[edit]

While shortness of breath is generally caused by disorders of the cardiac or respiratory system, other systems such as neurological,[10] musculoskeletal, endocrine, hematologic, and psychiatric may be the cause.[4] DiagnosisPro, an online medical expert system, listed 497 distinct causes in October 2010.[11] The most common cardiovascular causes are acute myocardial infarction and congestive heart failure while common pulmonary causes include chronic obstructive pulmonary disease, asthma, pneumothorax, pulmonary edema and pneumonia.[2] On a pathophysiological basis the causes can be divided into: (1) an increased awareness of normal breathing such as during an anxiety attack, (2) an increase in the work of breathing and (3) an abnormality in the ventilatory system.[10]

Acute coronary syndrome[edit]

Acute coronary syndrome frequently presents with retrosternal chest discomfort and difficulty catching the breath.[2] It however may atypically present with shortness of breath alone.[12] Risk factors include old age, smoking, hypertension, hyperlipidemia, and diabetes.[12] An electrocardiogram and cardiac enzymes are important both for diagnosis and directing treatment.[12] Treatment involves measures to decrease the oxygen requirement of the heart and efforts to increase blood flow.[2]

Congestive heart failure[edit]

Congestive heart failure frequently presents with shortness of breath with exertion, orthopnea, and paroxysmal nocturnal dyspnea.[2] It affects between 1-2% of the general United States population and occurs in 10% of those over 65 years old.[2][12] Risk factors for acute decompensation include high dietary salt intake, medication noncompliance, cardiac ischemia, dysrhythmias, renal failure, pulmonary emboli, hypertension, and infections.[12] Treatment efforts are directed towards decreasing lung congestion.[2]

Chronic obstructive pulmonary disease[edit]

People with chronic obstructive pulmonary disease (COPD), most commonly emphysema or chronic bronchitis, frequently have chronic shortness of breath and a chronic productive cough.[2] An acute exacerbation presents with increased shortness of breath and sputum production.[2] COPD is a risk factor for pneumothorax; thus this condition should be ruled out.[2] In an acute exacerbation treatment is with a combination of anticholinergics, beta2-adrenoceptor agonists, steroids and possibly positive pressure ventilation.[2]

Asthma[edit]

Asthma is the most common reason for presenting to the emergency with shortness of breath.[2] It is the most common lung disease in both developing and developed countries affecting about 5% of the population.[2] Other symptoms include wheezing, tightness in the chest, and a non productive cough.[2] Inhaled corticosteroids are the preferred treatment for children, however these drugs can reduce the growth rate.[13] Acute symptoms are treated with short-acting bronchodilators.

Pneumothorax[edit]

Main article: Pneumothorax

Pneumothorax presents typically with pleuritic chest pain of acute onset and shortness of breath not improved with oxygen.[2] Physical findings may include absent breath sounds on one side of the chest, jugular venous distension, and tracheal deviation.[2]

Pneumonia[edit]

Main article: Pneumonia

The symptoms of pneumonia are fever, productive cough, shortness of breath, and pleuritic chest pain.[2] Inspiratory crackles may be heard on exam.[2] A chest x-ray can be useful to differential pneumonia from congestive heart failure.[2] As the cause is usually a bacterial infections antibiotics are typically used for treatment.[2]

Important to remember: Severity and prognosis of Pneumonia can be estimated from CURB65, where C=Confusion, U= Uremia (>7), R=Respiratory rate >30, B= BP<90, 65= Age>65.

Pulmonary embolism[edit]

Pulmonary embolism classically presents with an acute onset of shortness of breath.[2] Other presenting symptoms include pleuritic chest pain, cough, hemoptysis, and fever.[2] Risk factors include deep vein thrombosis, recent surgery, cancer, and previous thromboembolism.[2] It must always be considered in those with acute onset of shortness of breath owing to its high risk of mortality.[2] Diagnosis however may be difficult.[2] Treatment is typically with anticoagulants.[2]

Anaemia[edit]

Anaemia caused by low hemoglobin levels is often a cause of dyspnea. Menstruation, particularly if excessive, can contribute to anaemia and to consequential dyspnea in women. Headaches are also a symptom of dyspnea in patients suffering from anaemia, some patients report a numb sensation in their head, and others have reported blurred vision caused by hypotension behind the eye due to a lack of oxygen and pressure, these patients have also reported severe head pain many of which lead to permanent brain damage, symptoms of this can be loss of concentration, focus, fatigue, language faculty impairment and memory loss.[citation needed]

Other[edit]

Other important or common causes of shortness of breath include cardiac tamponade, anaphylaxis, interstitial lung disease, panic attacks,[4][5][14] and pulmonary hypertension. Cardiac tamponade presents with dyspnea, tachycardia, elevated jugular venous pressure, and pulsus paradoxus.[14] The gold standard for diagnosis is ultrasound.[14] Anemia, that develops gradually, usually presents with exertional dyspnea, fatigue, weakness, and tachycardia.[14] It may lead to heart failure.[14] Anaphylaxis typically begins over a few minutes in a person with a previous history of the same.[5] Other symptoms include urticaria, throat swelling, and gastrointestinal upset.[5] The primary treatment is epinephrine.[5] Interstitial lung disease presents with gradual onset of shortness of breath typically with a history of a predisposing environmental exposure.[4] Shortness of breath is often the only symptom in those with tachydysrhythmias.[12] Panic attacks typically present with hyperventilation, sweating, and numbness.[5] They are however a diagnosis of exclusion.[4] Around 2/3 of women experience shortness of breath as a part of a normal pregnancy.[8] Neurological conditions such as spinal cord injury, phrenic nerve injuries, Guillain-Barre syndrome, amyotrophic lateral sclerosis, multiple sclerosis and muscular dystrophy can all cause an individual to experience shortness of breath.[10] A relatively unknown condition involving shortness of breath is empty nose syndrome.

Pathophysiology[edit]

Different physiological pathways may lead to shortness of breath including via chemoreceptors, mechanoreceptors, and lung receptors.[12]

It is thought that three main components contribute to dyspnea: afferent signals, efferent signals, and central information processing. It is believed the central processing in the brain compares the afferent and efferent signals; and dyspnea results when a "mismatch" occurs between the two: such as when the need for ventilation (afferent signaling) is not being met by physical breathing (efferent signaling).[15]

Afferent signals are sensory neuronal signals that ascend to the brain. Afferent neurons significant in dyspnea arise from a large number of sources including the carotid bodies, medulla, lungs, and chest wall. Chemoreceptors in the carotid bodies and medulla supply information regarding the blood gas levels of O2, CO2 and H+. In the lungs, juxtacapillary (J) receptors are sensitive to pulmonary interstitial edema, while stretch receptors signal bronchoconstriction. Muscle spindles in the chest wall signal the stretch and tension of the respiratory muscles. Thus, poor ventilation leading to hypercapnia, left heart failure leading to interstitial edema (impairing gas exchange), asthma causing bronchoconstriction (limiting airflow) and muscle fatigue leading to ineffective respiratory muscle action could all contribute to a feeling of dyspnea.[15]

Efferent signals are the motor neuronal signals descending to the respiratory muscles. The most important respiratory muscle is the diaphragm. Other respiratory muscles include the external and internal intercostal muscles, the abdominal muscles and the accessory breathing muscles.

As the brain receives its plentiful supply of afferent information relating to ventilation, it is able to compare it to the current level of respiration as determined by the efferent signals. If the level of respiration is inappropriate for the body's status then dyspnea might occur. There is also a psychological component to dyspnea, as some people may become aware of their breathing in such circumstances but not experience the distress typical of dyspnea.[15]

Evaluation[edit]

mMRC breathlessness scale
Grade Degree of dyspnea
0 no dyspnea except with strenuous exercise
1 dyspnea when walking up an incline or hurrying on the level
2 walks slower than most on the level, or stops after 15 minutes of walking on the level
3 stops after a few minutes of walking on the level
4 with minimal activity such as getting dressed, too dyspneic to leave the house

The initial approach to evaluation begins by assessment of the airway, breathing, and circulation followed by a medical history and physical examination.[2] Signs that represent significant severity include hypotension, hypoxemia, tracheal deviation, altered mental status, unstable dysrhythmia, stridor, intercostal indrawing, cyanosis, Tripod Positioning, pronounced use of accessory muscles (Sternocleidomastoid, Scalenes) and absent breath sounds.[4]

A number of scales may be used to quantify the degree of shortness of breath.[16] It may be subjectively rated on a scale from 1 to 10 with descriptors associated with the number (The Modified Borg Scale).[16] Alternatively a scale such as the MRC breathlessness scale might be used – it suggests five different grades of dyspnea based on the circumstances in which it arises.[17]

Blood tests[edit]

A number of labs may be helpful in determining the cause of shortness of breath. D-dimer while useful to rule out a pulmonary embolism in those who are at low risk is not of much value if it is positive as it may be positive in a number of conditions that lead to shortness of breath.[12] A low level of brain natriuretic peptide is useful in ruling out congestive heart failure; however, a high level while supportive of the diagnosis could also be due to advanced age, renal failure, acute coronary syndrome, or a large pulmonary embolism.[12]

Imaging[edit]

A chest x-ray is useful to confirm or rule out a pneumothorax, pulmonary edema, or pneumonia.[12] Spiral computed tomography with intravenous radiocontrast is the imaging study of choice to evaluate for pulmonary embolism.[12]

Treatment[edit]

In those who are not palliative the primary treatment of shortness of breath is directed at its underlying cause.[5] Extra oxygen is effective in those with hypoxia; however, this has no effect in those with normal blood oxygen saturations, even in those who are palliative.[3][18]

Physiotherapy[edit]

Individuals can benefit from a variety of physical therapy interventions.[19] Persons with neurological/neuromuscular abnormalities may have breathing difficulties due to weak or paralyzed intercostal, abdominal and/or other muscles needed for ventilation.[20] Some physical therapy interventions for this population include active assisted cough techniques,[21] volume augmentation such as breath stacking,[22] education about body position and ventilation patterns[23] and movement strategies to facilitate breathing.[22]

Palliative[edit]

Along with the measure above, systemic immediate release opioids are beneficial in emergently reducing the symptom of shortness of breath due to both cancer and non cancer causes;[3][24] long-acting/sustained-release opioids are also used to prevent/continue treatment of dyspnea in palliative setting. There is a lack of evidence to recommend midazolam, nebulised opioids, the use of gas mixtures, or cognitive-behavioral therapy.[25]

Epidemiology[edit]

Shortness of breath is the primary reason 3.5% of people present to the emergency department in the United States. Of these approximately 51% are admitted to hospital and 13% are dead within a year.[26] Some studies have suggested that up to 27% of people suffer from dyspnea,[27] while in dying patients 75% will experience it.[15] Acute shortness of breath is the most common reason people requiring palliative care visit an emergency department.[3]

Etymology[edit]

Dyspnea (/dɪspˈnə/ disp-NEE; from Latin dyspnoea, from Greek dyspnoia from dyspnoos) literally means disordered breathing.[4]

See also[edit]

References[edit]

  1. ^ About.com Health's Disease and Condition content > Dyspnea By Deborah Leader. Updated August 05, 2008
  2. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac Shiber JR, Santana J (May 2006). "Dyspnea". Med. Clin. North Am. 90 (3): 453–79. doi:10.1016/j.mcna.2005.11.006. PMID 16473100. 
  3. ^ a b c d e Schrijvers D, van Fraeyenhove F (2010). "Emergencies in palliative care". Cancer J 16 (5): 514–20. doi:10.1097/PPO.0b013e3181f28a8d. PMID 20890149. 
  4. ^ a b c d e f g Sarkar S, Amelung PJ (September 2006). "Evaluation of the dyspneic patient in the office". Prim. Care 33 (3): 643–57. doi:10.1016/j.pop.2006.06.007. PMID 17088153. 
  5. ^ a b c d e f g h Zuberi, T. et al. (2009). "Acute breathlessness in adults". InnovAiT 2 (5): 307–15. doi:10.1093/innovait/inp055. 
  6. ^ American Heart Society (1999). "Dyspnea mechanisms, assessment, and management: a consensus statement". Am Rev Resp Crit Care Med 159: 321–340. doi:10.1164/ajrccm.159.1.ats898. 
  7. ^ TheFreeDictionary, retrieved on Dec 12, 2009. Citing:The American Heritage Dictionary of the English Language, Fourth Edition by Houghton Mifflin Company. Updated in 2009.Ologies & -Isms. The Gale Group 2008
  8. ^ a b "UpToDate Inc.". 
  9. ^ "dyspnea – General Practice Notebook". 
  10. ^ a b c Frownfelter, Donna; Dean, Elizabeth (2006). "8". In Willy E. Hammon III. Cardiovascular and Pulmonary Physical Therapy 4. Mosby Elsevier. p. 139. 
  11. ^ http://en.diagnosispro.com/differential_diagnosis-for/poisoning-specific-agent-dyspnea/25103-154-100.html
  12. ^ a b c d e f g h i j k Torres M, Moayedi S (May 2007). "Evaluation of the acutely dyspneic elderly patient". Clin. Geriatr. Med. 23 (2): 307–25, vi. doi:10.1016/j.cger.2007.01.007. PMID 17462519. 
  13. ^ "How Is Asthma Treated and Controlled?". 
  14. ^ a b c d e Wills CP, Young M, White DW (February 2010). "Pitfalls in the evaluation of shortness of breath". Emerg. Med. Clin. North Am. 28 (1): 163–81, ix. doi:10.1016/j.emc.2009.09.011. PMID 19945605. 
  15. ^ a b c d Harrison's Principles of Internal Medicine (Kasper DL, Fauci AS, Longo DL, et al (eds)) (16th ed.). New York: McGraw-Hill.
  16. ^ a b Saracino A (October 2007). "Review of dyspnoea quantification in the emergency department: is a rating scale for breathlessness suitable for use as an admission prediction tool?". Emerg Med Australas 19 (5): 394–404. doi:10.1111/j.1742-6723.2007.00999.x. PMID 17919211. 
  17. ^ Stenton C (2008). "The MRC breathless scale". Occup Med 58 (3): 226–7. doi:10.1093/occmed/kqm162. PMID 18441368. 
  18. ^ Abernethy AP, McDonald CF, Frith PA et al. (September 2010). "Effect of palliative oxygen versus medical (room) air in relieving breathlessness in patients with refractory dyspnea: a double-blind randomized controlled trial". Lancet 376 (9743): 784–93. doi:10.1016/S0140-6736(10)61115-4. PMC 2962424. PMID 20816546. 
  19. ^ Frownfelter, Donna; Dean, Elizabeth (2006). "8". In Willy E. Hammon III. Cardiovascular and Pulmonary Physical Therapy 4. Mosby Elsevier. 
  20. ^ Frownfelter, Donna; Dean, Elizabeth (2006). "22". In Donna Frownfelter and Mary Massery. Cardiovascular and Pulmonary Physical Therapy 4. Mosby Elsevier. p. 368. 
  21. ^ Frownfelter, Donna; Dean, Elizabeth (2006). "22". In Donna Frownfelter and Mary Massery. Cardiovascular and Pulmonary Physical Therapy 4. Mosby Elsevier. pp. 368–371. 
  22. ^ a b Frownfelter, Donna; Dean, Elizabeth (2006). "32". Cardiovascular and Pulmonary Physical Therapy 4. Mosby Elsevier. pp. 569–581. 
  23. ^ Frownfelter, Donna; Dean, Elizabeth (2006). "23". In Donna Frownfelter and Mary Massery. Cardiovascular and Pulmonary Physical Therapy 4. Mosby Elsevier. 
  24. ^ Naqvi F, Cervo F, Fields S (August 2009). "Evidence-based review of interventions to improve palliation of pain, dyspnea, depression". Geriatrics 64 (8): 8–10, 12–4. PMID 20722311. 
  25. ^ DiSalvo, WM.; Joyce, MM.; Tyson, LB.; Culkin, AE.; Mackay, K. (Apr 2008). "Putting evidence into practice: evidence-based interventions for cancer-related dyspnea" (PDF). Clin J Oncol Nurs 12 (2): 341–52. doi:10.1188/08.CJON.341-352. PMID 18390468. 
  26. ^ Stephen J. Dubner; Steven D. Levitt (2009). SuperFreakonomics: Tales of Altruism, Terrorism, and Poorly Paid Prostitutes. New York: William Morrow. p. 77. ISBN 0-06-088957-8. 
  27. ^ Murray and Nadel's Textbook of Respiratory Medicine, 4th Ed. Robert J. Mason, John F. Murray, Jay A. Nadel, 2005, Elsevier

External links[edit]