You are on page 1of 4

Dyspnea is an uncomfortable abnormal awareness of breathing.

A number of different
sensations experienced by patients are probably included in this category. Dyspnea is the
most common cause of respiratory limitation of activity in patients with pulmonary disease.

Dyspnea is a subjective symptom reported by patients. It is always a sensation expressed by


the patient and should not be confused with rapid breathing (tachypnea), excessive breathing
(hyperpnea), or hyperventilation. Dyspnea is most frequently described as shortness of
breath, inability to take a deep breath, or chest tightness.

The sensations produced in normal people by the above experiments are probably not the
same, even though they frequently are lumped into the single category of dyspnea. Similarly,
it is probable that patients with complaints of dyspnea do not all have identical sensations.
Dyspnea is a common complaint in patients with obstructive and restrictive pulmonary
disorders. In addition, patients with chest wall abnormalities such as kyphoscoliosis and
patients with neuromuscular disease frequently complain of dyspnea. What the mechanisms
for these various dyspneic sensations are is not completely clear.

Mechanism of dyspnea

Most diseases associated with dyspnea are accompanied by an abnormality in pulmonary


mechanics with a subsequent increase in the overall work of breathing. The increased work of
breathing may be due to an increase in elastic work (restrictive disease) or resistive work
(obstructive disease). The conscious perception of dyspnea probably results from a
complicated interrelationship of peripheral receptors, neural pathways, and the central
nervous system. The peripheral receptors most commonly implicated include receptors in the
chest wall associated with the respiratory muscle spindles, receptors in the pulmonary
parenchyma, receptors in the central airways, and chemoreceptors such as the carotid body.
The connecting neural pathways include the vagi and afferent neurons in the spinal cord. The
central neural mechanisms include central chemoreceptors, inspiratory neurons in the
medulla, and higher cortical centers. Whenever these mechanisms produce an overall
respiratory pattern where an increased requirement for ventilation is balanced by an expected
increase in respiratory output, no sensation of abnormal breathing occurs. When respiratory
output is in some way inappropriate for ventilation requirements, the conscious sensation of
this inappropriateness results in the sensation of dyspnea.

In this learning issue we talk about progressive(worsening) dyspnea. What does progressive
dyspnea mean? By progressive here it means the difficulty and uncomfortness of breathing is
worsening gradually. If remain untreated, it may lead to breathing failure and eventually
death. The progress may take several days, weeks, months or years, also it may happen in a
emergency case which only last a few hours and need immadiate treatment. Below we will
list some disease and abnormalities which involve progressive dyspnea.
Type of dyspnea

Dyspnea can be symptomatic of a variety of disorders, both acute and chronic. Acute
conditions include acute infections and inflammations of the respiratory tract, obstruction by
an inhaled foreign object, anaphylactic swelling of the tracheal and bronchial mucosa, and
traumatic injury to the chest. Chronic disorders usually fall into the category of Chronic
Airflow Limitation, or are associated with pulmonary edema and congestive heart failure. A
fat embolism resulting from the release of fat particles from bone marrow at the time of a
fracture of a long bone also can cause dyspnea

Acute shortness of breath, which comes on suddenly, over the course of minutes or hours,
usually has different causes than chronic shortness of breath, which develops over weeks or
months. The most common causes of acute shortness of breath involving worsening dyspnea
include:

 Respiratory muscle abnormalities. Weakness or mechanical inefficiency of the


respiratory muscles results in a mismatch between central respiratory motor output
and achieved ventilation. This mismatch may explain the dyspnea experienced by
patients with neuromuscular diseases affecting the respiratory musculature and
patients with respiratory muscle fatigue. As the pressure-generating capacity of the
respiratory muscles fall and as the ratio of the pressures produced by the respiratory
muscles to the maximum pressure that can be achieved increases, dyspnea
progressively worsen.

 A collapsed lung (pneumothorax)


A pneumothorax (pneumo- + thorax; plural pneumothoraces) is an
abnormal collection of air or gas in the pleural space that separates the lung from the
chest wall. Like pleural effusion (liquid buildup in that space), pneumothorax may
interfere with normal breathing. It is often called collapsed lung, although that term
may also refer to atelectasis.
A primary pneumothorax is one that occurs without an apparent cause and
in the absence of significant lung disease, while a secondary pneumothorax occurs
in the presence of existing lung pathology. In a minority of cases, the amount of air in
the chest increases markedly when a one-way valve is formed by an area of damaged
tissue, leading to a tension pneumothorax. This condition is a medical emergency
that can cause steadily worsening oxygen shortage and low blood pressure. Unless
reversed by effective treatment, these sequelae can progress and cause death.
Pneumothoraces can be caused by physical trauma to the chest (including blast
injury), or as a complication of medical or surgical intervention. Symptoms typically
include chest pain and shortness of breath. Diagnosis of a pneumothorax by physical
examination alone can be difficult or inconclusive (particularly in smaller
pneumothoraces), so a chest X-ray or computed tomography (CT) scan is usually used
to confirm its presence.
 Heart failure, a condition that affects the heart's ability to pump blood throughout the
body. Congestive heart failure, when acute, may be associated with myocardial
infarction. Chronic congestive heart failure is associated with a number of myocardial
diseases. Patients with congestive heart failure frequently present with progressive
dyspnea, orthopnea, and peripheral edema
 A severe allergic reaction (anaphylaxis), which usually also causes itching, swelling, a
rash, or other symptoms.
 Asthma, which often causes wheezing.
 A blockage in the respiratory tract, which could happen after accidentally inhaling a
foreign object, such as a peanut or partially chewed meat.

Chronic shortness of breath — Some of the same things that cause acute shortness of breath
can also cause chronic shortness of breath. For example, asthma symptoms can come and go
over months or years. Heart failure can also continue to cause shortness of breath over
months or years.The most common causes of chronic shortness of breath include:

 Asthma
 Chronic Obstructive Pulmonary Disease
A few of the most common disorders are outlined here. Patients with chronic
obstructive pulmonary disease (COPD), which comprises emphysema and chronic
bronchitis, generally present with a long history of cigarette smoking and gradually
progressive dyspnea over a number of years. Pulmonary function abnormalities
frequently progress for years before clinical dyspnea occurs. Most patients do not
have day-to-day variation in their symptoms, but they may have exacerbations during
the winter months. A productive cough is a frequent associated symptom, and the
sputum may become purulent during exacerbations.
 Interstitial lung disease, a collection of lung disorders that involve damage or
scarring of lung tissue. Patients with pulmonary fibrosis generally present with
progressive and relentless dyspnea with a variable time course. Frequently the only
associated symptom is a non-productive cough. Extrapulmonary manifestations of
diseases associated with pulmonary fibrosis may be present. The occupational and
environmental history is particularly important.
Mahler DA, O'Donnell DE. 2014. Dyspnea: Mechanisms, Measurement, and Management.
3rd Edition. NW: CRC Press. p. 3.

Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh
Edition. 2003. Saunders, Elsevier, Inc.

Bass JB JR. 1990. Dyspnea. In Walker HK, Hall WD, Hurst JW (Eds.). Clinical Methods:
The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths.
Chapter 36. Available from: http://www.ncbi.nlm.nih.gov/books/NBK357/

Noppen M, De Keukeleire T. 2008. Pneumothorax. Respiration;76:121-127

Tschopp J-M., Rami-Porta R. , Noppen M., Astoul P. 2006. Management of spontaneous


pneumothorax: state of the art. European Respiratory Journal; 28: 637–650.