by Alberto J. Muniagurria and Juan Carlos Daltio
It is the subjective, unpleasant feeling of shortness of breath. This defines it as a pure symptom, in the field of perceptions, and therefore is not always accompanied by obvious objective alterations.
Dyspnea must be distinguished: from tachypnea or polypnea , which is the increase in respiratory rate; the hyperpnea , which refers to the increase in frequency and depth of breathing, and bradipnea , defining decreased respiratory rate.
Pathophysiology. Dyspnea occurs when the demand for ventilation is disproportionate in relation to the patient's capacity to respond to said demand. As a consequence, breathing is difficult, uncomfortable, or forced.
An increased demand for ventilation is caused by changes in blood gases and pH. Thus, an increase in ventilation is observed in patients with deficiency in the exchange of pulmonary gases, especially those with large physiological dead spaces, which tend to retain C0 2 and acidosis. However, the difficulty in fully explaining the pathophysiology through the aforementioned mechanism lies in the fact, of frequent observation, of the existence of abnormalities in the concentrations of 0 2 and C0 2in the blood without manifestations of dyspnea, and conversely, of dyspneic patients with normal blood gases. Another factor is stimulation of intrapulmonary stretch receptors. Dyspnea, in this case, results from the alterations between the force applied to the lung and the movement it causes, so that the resulting ventilation does not match the demand of the respiratory centers.
The capacity reduced response to the needs of ventilation should be, usually, to an abnormal mechanics of the lung or chest wall. The most frequent etiological factor is the increased resistance of the airways, as observed in asthma. Another cause is stiff chest wall that occurs in kyphoscoliosis.
A third mechanism would be the excessive awareness of the act of breathing ; for example, in the neurotic patient.
Therefore, dyspnea occurs whenever the respiratory work is excessive.
Causes of dyspnea
Most of the patients who consult for this symptom fall into the following groups:
- Obstructive pulmonary disease
- Interstitial and / or alveolar lung disease
- Chest wall or respiratory muscle disease
- Circulation disorders
- Neurosis of anxiety. Hysteria.
Obstructive pulmonary disease. Asthma is the bronchial pathology that most often produces dyspnea. It has some special characteristics, such as sudden onset, great expiratory difficulty, abundant adhesive mucous secretion difficult to expectorate, chronic evolution with frequent acute exacerbations, leafy allergic history and sequelae after years of evolution.
This table identifies one of the classes of dyspnea that is called paroxysmal. The other obstructive diseases that cause dyspnea are pulmonary emphysema, chronic bronchitis, recurrent infections, etc. Here dyspnea appears with exertion, in the early stages only in relation to tasks that demand greater oxygen consumption, but as the lung loses its normal structure, the symptom will appear before habitual efforts such as walking, until finally A permanent dyspnea will be installed that is maintained even during rest.
Diseases of the interstitium and pulmonary alveolus, This chapter includes countless pathologies, which have in common the loss of lung elasticity with thickening of the interalveolar septa, alterations of the endothelium and, as a consequence, disorders in gas exchange; therefore, dyspnea has to occur at some point in evolution. Because the diseases that affect this sector can be infectious (virus, Pneumocystis carinii, etc.) or immunological (idiopathic fibrosis), and since they evolve chronically, progressively affecting the entire lung, dyspnea will also progressively settle in time and may even become permanent. Passive congestion, of cardiac cause, which will be considered within dyspnea of cardiovascular cause, is excluded from this group.
Diseases of the chest wall and respiratory muscles. Firstly, fractures of one or several ribs are included, which, by preventing a correct thoracic expansion, are responsible for dyspnea. The intense pain caused by respiratory movements causes the patient to try to immobilize the chest and perform a purely diaphragmatic breathing, which is not always sufficient for proper ventilation.
Poliomyelitis muscle paralysis and Landry's ascending paralysis, causing loss of muscle strength in the chest, cause dyspnea with severe hypoventilation that requires assisted breathing.
Although they do not constitute pathology of the chest wall, but by sharing with it the decrease in expansion, large pleural effusions (serous, purulent or hematic) are included in this group, as factors that significantly limit breathing and produce dyspnea. In this case, the appearance and progression of dyspnea will be determined by the magnitude of the displaced lung. Do not forget pneumothorax, which, if it is total, will be the cause of sudden paroxysmal dyspnea, which will decrease as the affected lung re-expands.
Circulatory diseases (cardiovascular) . Left heart failure, by causing a blood removal in the lung, triggers a picture of paroxysmal nocturnal dyspnea that accompanies acute lung edema. The sequence of events would be: a) increase in venous return by reabsorption of edema during rest; b) ventricular failure to manage this excess effective volume having lost its functional reserve; c) pulmonary and capillary venous hypertension; d) transudation into the alveoli, and e) ventilatory failure.
The patient spontaneously sits on the bed (orthopnea) to decrease the venous return and thus relieve dyspnea.
Another cardiac condition that causes dyspnea is mitral stenosis, which by a similar mechanism generates pulmonary congestion; As it is a
constant obstruction to atrioventricular blood flow, dyspnea in this case will not be paroxysmal but permanent, and will evolve according to the degree of valve tightness.
Nervous dyspnea. In this group that is difficult to classify but is very frequent, patients whose reason for consultation is "shortness of breath" are included, in which the doctor, through physical examination and complementary studies, cannot detect obvious organic pathology to justify the symptom. Among the psychological symptoms that most commonly present dyspnea, are conversion hysteria and anxiety neurosis, where the patient perceives insufficient breathing, which in turn increases anxiety and anxiety, making it difficult get out of this vicious circle that makes you control your breathing voluntarily. The most outstanding characteristic of this group is that it forms an atypical dyspnea unrelated to effort, positions, rest, schedules or meals,
Dyspnea can be classified according to its duration, intensity, causes, and body position in which it appears and time or circumstance of appearance.
Regarding its duration, it is divided into permanent dyspnea and non-permanent dyspnea. The permanent dyspnea is the heritage of acute and chronic respiratory failure in advanced stages of major trauma ios thoracic, and pneumothorax and hemothorax. It can also be seen in pulmonary microembolism.
The non - permanent dyspnoea can be divided, by way of beginning, paroxysmal , such as acute pulmonary edema and stress, when it appears with movements of variable magnitude. Paroxysmal nocturnal dyspnea, also known as cardiac asthma, is characterized by presenting at night. The patient wakes up with severe respiratory distress. As already noted, the pathophysiology that explains this table is the increase in blood volume by reabsorption of the edema when the individual adopts the recumbent position. If this situation persists and increases, it can evolve into acute lung edema. It is accompanied by bronchospasm with wheezing. Unlike bronchial asthma, there is a history of underlying heart disease, head sweating, inspiratory and expiratory crackles that change with cough, and the presence of cyanosis is more common.
Effort dyspnea, in turn, can be quantified in degrees of intensity: degree I is that which appears with the great efforts to which the individual is accustomed, such as running, sports competitions, etc .; Grade II is that presented with moderate efforts, for example, walking, grade III: manifests itself in minimal efforts such as dressing and combing.
Due to its causes, dyspnea is divided into respiratory and cardiac ; while due to the body position in which it appears, it is classified into orthopnea, trepopnea and platypnea.
The ortopnea is a characteristic dyspnea recumbency heart failure, and is, in general, a manifestation of more advanced heart failure exertional dyspnea. Its origin is in the redistribution of blood in the decubitus position, which increases the effective blood volume which in turn increases the venous and pulmonary capillary pressure due to the insufficient pumping capacity of the left ventricle. Simultaneously, a diaphragmatic elevation occurs with the consequent alteration of the ventilation of the pulmonary bases.
The trepopnea characterized by difficulty breathing in both lateral decubitus. It is observed in cardiac diseases and in pleural effusions, when the patient lies decubitus opposite to the effusion. The platypnea , finally, is dyspnea appears in a standing position.
Through questioning, sufficient information must be obtained to guide the diagnosis:
- Evolution time (since when?)
- Time of appearance (doing what?)
- Relationship with effort
- Relationship with rest (whether calm or not)
- Progression over time (in intensity and duration)
- Abrupt or progressive onset
- Duration of the crisis
- Interval duration
- Relationship to position
- Concomitant symptoms (pain, cough)
- Concomitant signs (expectoration, diaphoresis, pallor, cyanosis, etc.)
Other respiratory disorders
The Kussmaul breathing is shown in metabolic acidosis, in which, to be increased the amount of hydrogen ions, the respiratory center reacts by increasing the number and depth of breathing; This situation is not necessarily accompanied by labored breathing.
The Biot breathing is seen in severe injuries of the central nervous system (viral encephalitis, stroke). It consists of breathing with low respiratory rate and prolonged apneic pauses, which maintains a certain regularity.
The Cheyne-Stokes respiration is characterized by a prolonged apneic pause and then a progression of inspirations in crescendo, then they go to decrease until a new apneic pause occurs, and so on. It is also called periodic breathing, a phenomenon that can occur in heart failure and in intracranial hypertension.
The respiratory ataxia is free breathing rate or regularity, where apneic phases occur with protracted periods of hyperpnea variable depth. It appears in the deepest stages of coma, and speaks of the failure of the respiratory center to maintain adequate ventilation. They are always seriously ill, whose condition is rarely reversible.