STUDY - Technical - New Dacian's Medicine
Dyspnoea
and Pulmonary Edema (1)
Translation Draft
According to the title, I'll start with dyspnea. Breathing is under the control of superior and peripheral central mechanisms, which can regulate ventilation according to increased metabolic needs during physical activity. It can also increase ventilation over metabolic needs in conditions such as anxiety and fear. In conditions of normal relaxation, a person is not aware of the respiratory act, but may become aware of this act under conditions of light or moderate exertion without trying a state of discomfort.
However, under conditions of effort or after effort, an individual may become unpleasantly aware of the respiratory act, but is assured that it is a transient act, appropriate to the effort it makes. Therefore, as the main symptom of diseases affecting the cardiorespiratory system, dyspnea is defined as an uncomfortable and abnormal state of awareness of breathing.
Although dyspnea is not painful in the usual sense of the word, it implies, like pain, both the perception of sensation and the reaction to this perception. Patients describe these breathing-related discomforts in different ways and use a large number of verbal expressions to describe them, such as "no air", "air not coming down enough", "a feeling of pressure, tightness or tiredness in the chest", "feeling suffocated", etc.
Therefore, a meticulous resumption of the patient's disease history may be necessary to see exactly whether the patient's most confusing descriptions actually represent dyspnea. Once established that the patient has dyspnea, it is extremely important to define under what conditions it occurs and what are the associated symptoms. There are times when breathing seems laborious, but dyspnea is not present. For example, hyperventilation associated with metabolic acidosis is rarely accompanied by dyspnea. On the other hand, patients who apparently have normal breathing may complain of a "shortness" of breathing.
Now, a little bit about quantifying dyspnea. The gradation of dyspnea can be usefully based on the amount of physical exertion required to produce this sensation. However, in order to affirm the severity of dyspnea, it is important to understand the patient's physical condition, work history and recreational habits.
For example, the development of dyspnea in a runner trained after running 3 km may mean more of a serious disorder than a similar degree of loss of breath in a sedentary person after running a fraction of this distance. Individual variation in perception should also be taken into account.
Some patients with severe illness may experience only mild breathlessness, others with a mild form of the disease may suffer more severe breathing impairments. There are patients who have lung or heart disease and who have such reduced capacities due to other diseases (e.g. peripheral vascular insufficiency or a severe form of osteoarthritis of the hip or knees) that exercise dyspnea is excluded, despite serious damage to lung or cardiac function. Some types of dyspnea are not directly related to physical exertion.
Spontaneous and sudden dyspneic episodes at rest may be associated with pulmonary embolism, pneumothorax, hypercapnia secondary to voluntary cessation of breathing or anxiety. Nocturnal episodes of severe paroxysmal dyspnea are characteristic of left ventricular insufficiency.
Dyspnea in clinostatism, ortopnea, considered to be the main feature of congestive heart failure, may also occur in some patients with asthma and chronic airway obstruction and is a characteristic sign in the rare cases of bilateral diaphragmatic paralysis.
Trepopnea is used to describe unusual circumstances in which dyspnea occurs only in the right or left lateral decubit position, most often in patients with heart disease, while platipnea is dyspnea that occurs only in the orthostatic position. Positional changes in ventilation-perfusion relationships have been invoked to explain these types of dyspnea.
Platipnea can also be observed in the case of defective abdominal muscles, a deficiency that results in loss of diaphragmatic support due to the previous displacement of the abdominal viscera in the orthostatic position. In the lying position, the viscera resume the supporting role of the diaphragm, which returns to the optimal operational length. This form of platipnea is improved by the use of an abdominal belt.
Now let's see what the mechanisms of dyspnea are. Doctors usually correlate symptoms of dyspnea with a process such as airway obstruction or congestive heart failure and generally continue with subsequent diagnosis and/ or therapeutic tests, content for understanding the mechanism of dyspnea.
In fact, elucidating the actual mechanisms of dyspnea has circumvented clinical investigations. Dyspnea occurs whenever the respiratory act is excessive. It is necessary to generate greater forces in the respiratory muscles to produce a change in a given volume if the chest wall or lungs are less compliant or if resistance to air penetration is increased.
Also, increased breathing activity occurs when ventilation is excessive for the level of activity. Although an individual is potentially dyspneic when breathing, effort theory does not give information about a perceptible difference between deep breathing with a normal mechanical load and normal breathing with an increased mechanical load.
The effort may be the same in both cases, but the most normal with increased pregnancy will be associated with discomfort. In fact, respiratory loading, such as adding an obstacle to the mouth, leads to an increase in the activity of the respiratory center, which is disproportionate to the increase in respiratory effort.
It has been postulated that whenever the force actually generated by the muscles during breathing approaches a certain fraction of their maximum ability to generate force, which varies from individual to individual, dyspnea results from the transformation of mechanical stimuli into nervous stimuli.
Such a theory still would not explain why patients who are completely paralyzed, either by transverse bone marrow sectioning or neuromuscular blockage, get dyspnea, even though they are passed on assisted breathing.
In these circumstances, signals from the lung and/ or airways are likely to reach through the vagus nerve to the central nervous system and produce this sensation. With high probability, several different mechanisms participate to varying degrees in the various clinical situations in which dyspnea is present.
Under certain conditions, dyspnea is produced by stimulating receptors in the upper respiratory tract and in other patients, it may originate in receptors in the lungs, airways, respiratory muscles or some combinations of these structures.
In any case, dyspnea is characterized by abnormal or excessive activity of the respiratory centers in the brain stem. This activation comes from stimuli transmitted from or through a variety of structures and pathways, including: 1. intraoracic receptors through vague nerves, 2. somatic nerves afesing mainly from the respiratory muscles and chest wall, but also from other skeletal muscles and joints, 3. chemoreceptors in the brain, aortic and carotid walls and other parts of circulation, 4. centers (cortical) superior and probably 5. related fibers of the frenic nerves.
In general, despite the individual variations described above, there is a reasonable correlation between the severity of dyspnea and the extent of the disorders of cardiac or pulmonary function that cause it. The mechanisms responsible for the development of dyspnea may vary depending on the condition.
In asthma the mechanism is represented by increased sensitivity to exertion and stimulation of the irritation receptor in the airways, in neuromuscular diseases of increased sensitivity to exertion, in COPD (chronic obstructive pulmonary disease) the mechanism is represented by increased sensitivity to exertion, hypoxia, hypercapnia and dynamic compression of the airways, in the mechanical ventilation of the related inconsistency and factors associated with the base state and in the pulmonary embolism of stimulating pressure receptors in the pulmonary vessels or in the right atrium.
From the point of view of differential diagnosis I will start with obstructive airway disease. Obstruction to air ingress can be present anywhere, from the extrathoracic airways to those on the periphery of the lung.
A large extrathoracic obstruction of the airways can occur suddenly with inhalation of food or a foreign body or through the angioedema of the bullet. Testimonies of present persons and circumstantial data may cause the doctor to suspect aspiration, and a history of allergy along with urticariaskin skin manifestations should increase the possibility of glotic edema.
The acute form of upper airway obstruction is a medical emergency. Chronic forms may occur in the case of tumors or in fibrous stenosis after tracheostomy or after long-lasting endotracheal intubation. Whether it is a chronic case or an acute one, the main symptom is dyspnea, and the characteristic signs are the stridor and the retracement of the supraclavicular fossa in the breath.
Obstruction of the intraoracic airways may occur acutely and intermittently or may be chronically present with aggravation during respiratory infections. Acute intermittent obstruction with wheezing is typical of asthma. Chronic cough with expectoration is typical of chronic bronchitis and bronchitis. Most often a prolonged exhalation occurs and rough rals, generalized in chronic bronchitis and can be localized in case of bronchitis. Intercurrent infection causes worsening of the cough, abundant expectoration with purulent sputum and more severe dyspnea.
During such episodes, the patient may experience nocturnal paroxysmal dyspnoea with wheezing, relieved of coughing and expectoration. Despite the fact that severe limitation of exhaling flow and hyperinflation of the lung are characteristic of these diseases, the patient has the feeling that he cannot draw air into the lungs deep enough, rather than that he has difficulty in exhalation.
The patient with predominant emphysema is characterized by a dyspnea at exertion for several years, which progresses to dyspnea at rest. Although it is a parenchymal disease by definition, emphysema is invariably accompanied by airway obstruction.
I'm going to continue tomorrow with the differential diagnosis of dyspnea and address pulmonary edema.
A good, pleasant and spornic weekend, full of understanding, love and gratitude!
According to the title, I'll start with dyspnea. Breathing is under the control of superior and peripheral central mechanisms, which can regulate ventilation according to increased metabolic needs during physical activity. It can also increase ventilation over metabolic needs in conditions such as anxiety and fear. In conditions of normal relaxation, a person is not aware of the respiratory act, but may become aware of this act under conditions of light or moderate exertion without trying a state of discomfort.
However, under conditions of effort or after effort, an individual may become unpleasantly aware of the respiratory act, but is assured that it is a transient act, appropriate to the effort it makes. Therefore, as the main symptom of diseases affecting the cardiorespiratory system, dyspnea is defined as an uncomfortable and abnormal state of awareness of breathing.
Although dyspnea is not painful in the usual sense of the word, it implies, like pain, both the perception of sensation and the reaction to this perception. Patients describe these breathing-related discomforts in different ways and use a large number of verbal expressions to describe them, such as "no air", "air not coming down enough", "a feeling of pressure, tightness or tiredness in the chest", "feeling suffocated", etc.
Therefore, a meticulous resumption of the patient's disease history may be necessary to see exactly whether the patient's most confusing descriptions actually represent dyspnea. Once established that the patient has dyspnea, it is extremely important to define under what conditions it occurs and what are the associated symptoms. There are times when breathing seems laborious, but dyspnea is not present. For example, hyperventilation associated with metabolic acidosis is rarely accompanied by dyspnea. On the other hand, patients who apparently have normal breathing may complain of a "shortness" of breathing.
Now, a little bit about quantifying dyspnea. The gradation of dyspnea can be usefully based on the amount of physical exertion required to produce this sensation. However, in order to affirm the severity of dyspnea, it is important to understand the patient's physical condition, work history and recreational habits.
For example, the development of dyspnea in a runner trained after running 3 km may mean more of a serious disorder than a similar degree of loss of breath in a sedentary person after running a fraction of this distance. Individual variation in perception should also be taken into account.
Some patients with severe illness may experience only mild breathlessness, others with a mild form of the disease may suffer more severe breathing impairments. There are patients who have lung or heart disease and who have such reduced capacities due to other diseases (e.g. peripheral vascular insufficiency or a severe form of osteoarthritis of the hip or knees) that exercise dyspnea is excluded, despite serious damage to lung or cardiac function. Some types of dyspnea are not directly related to physical exertion.
Spontaneous and sudden dyspneic episodes at rest may be associated with pulmonary embolism, pneumothorax, hypercapnia secondary to voluntary cessation of breathing or anxiety. Nocturnal episodes of severe paroxysmal dyspnea are characteristic of left ventricular insufficiency.
Dyspnea in clinostatism, ortopnea, considered to be the main feature of congestive heart failure, may also occur in some patients with asthma and chronic airway obstruction and is a characteristic sign in the rare cases of bilateral diaphragmatic paralysis.
Trepopnea is used to describe unusual circumstances in which dyspnea occurs only in the right or left lateral decubit position, most often in patients with heart disease, while platipnea is dyspnea that occurs only in the orthostatic position. Positional changes in ventilation-perfusion relationships have been invoked to explain these types of dyspnea.
Platipnea can also be observed in the case of defective abdominal muscles, a deficiency that results in loss of diaphragmatic support due to the previous displacement of the abdominal viscera in the orthostatic position. In the lying position, the viscera resume the supporting role of the diaphragm, which returns to the optimal operational length. This form of platipnea is improved by the use of an abdominal belt.
Now let's see what the mechanisms of dyspnea are. Doctors usually correlate symptoms of dyspnea with a process such as airway obstruction or congestive heart failure and generally continue with subsequent diagnosis and/ or therapeutic tests, content for understanding the mechanism of dyspnea.
In fact, elucidating the actual mechanisms of dyspnea has circumvented clinical investigations. Dyspnea occurs whenever the respiratory act is excessive. It is necessary to generate greater forces in the respiratory muscles to produce a change in a given volume if the chest wall or lungs are less compliant or if resistance to air penetration is increased.
Also, increased breathing activity occurs when ventilation is excessive for the level of activity. Although an individual is potentially dyspneic when breathing, effort theory does not give information about a perceptible difference between deep breathing with a normal mechanical load and normal breathing with an increased mechanical load.
The effort may be the same in both cases, but the most normal with increased pregnancy will be associated with discomfort. In fact, respiratory loading, such as adding an obstacle to the mouth, leads to an increase in the activity of the respiratory center, which is disproportionate to the increase in respiratory effort.
It has been postulated that whenever the force actually generated by the muscles during breathing approaches a certain fraction of their maximum ability to generate force, which varies from individual to individual, dyspnea results from the transformation of mechanical stimuli into nervous stimuli.
Such a theory still would not explain why patients who are completely paralyzed, either by transverse bone marrow sectioning or neuromuscular blockage, get dyspnea, even though they are passed on assisted breathing.
In these circumstances, signals from the lung and/ or airways are likely to reach through the vagus nerve to the central nervous system and produce this sensation. With high probability, several different mechanisms participate to varying degrees in the various clinical situations in which dyspnea is present.
Under certain conditions, dyspnea is produced by stimulating receptors in the upper respiratory tract and in other patients, it may originate in receptors in the lungs, airways, respiratory muscles or some combinations of these structures.
In any case, dyspnea is characterized by abnormal or excessive activity of the respiratory centers in the brain stem. This activation comes from stimuli transmitted from or through a variety of structures and pathways, including: 1. intraoracic receptors through vague nerves, 2. somatic nerves afesing mainly from the respiratory muscles and chest wall, but also from other skeletal muscles and joints, 3. chemoreceptors in the brain, aortic and carotid walls and other parts of circulation, 4. centers (cortical) superior and probably 5. related fibers of the frenic nerves.
In general, despite the individual variations described above, there is a reasonable correlation between the severity of dyspnea and the extent of the disorders of cardiac or pulmonary function that cause it. The mechanisms responsible for the development of dyspnea may vary depending on the condition.
In asthma the mechanism is represented by increased sensitivity to exertion and stimulation of the irritation receptor in the airways, in neuromuscular diseases of increased sensitivity to exertion, in COPD (chronic obstructive pulmonary disease) the mechanism is represented by increased sensitivity to exertion, hypoxia, hypercapnia and dynamic compression of the airways, in the mechanical ventilation of the related inconsistency and factors associated with the base state and in the pulmonary embolism of stimulating pressure receptors in the pulmonary vessels or in the right atrium.
From the point of view of differential diagnosis I will start with obstructive airway disease. Obstruction to air ingress can be present anywhere, from the extrathoracic airways to those on the periphery of the lung.
A large extrathoracic obstruction of the airways can occur suddenly with inhalation of food or a foreign body or through the angioedema of the bullet. Testimonies of present persons and circumstantial data may cause the doctor to suspect aspiration, and a history of allergy along with urticariaskin skin manifestations should increase the possibility of glotic edema.
The acute form of upper airway obstruction is a medical emergency. Chronic forms may occur in the case of tumors or in fibrous stenosis after tracheostomy or after long-lasting endotracheal intubation. Whether it is a chronic case or an acute one, the main symptom is dyspnea, and the characteristic signs are the stridor and the retracement of the supraclavicular fossa in the breath.
Obstruction of the intraoracic airways may occur acutely and intermittently or may be chronically present with aggravation during respiratory infections. Acute intermittent obstruction with wheezing is typical of asthma. Chronic cough with expectoration is typical of chronic bronchitis and bronchitis. Most often a prolonged exhalation occurs and rough rals, generalized in chronic bronchitis and can be localized in case of bronchitis. Intercurrent infection causes worsening of the cough, abundant expectoration with purulent sputum and more severe dyspnea.
During such episodes, the patient may experience nocturnal paroxysmal dyspnoea with wheezing, relieved of coughing and expectoration. Despite the fact that severe limitation of exhaling flow and hyperinflation of the lung are characteristic of these diseases, the patient has the feeling that he cannot draw air into the lungs deep enough, rather than that he has difficulty in exhalation.
The patient with predominant emphysema is characterized by a dyspnea at exertion for several years, which progresses to dyspnea at rest. Although it is a parenchymal disease by definition, emphysema is invariably accompanied by airway obstruction.
I'm going to continue tomorrow with the differential diagnosis of dyspnea and address pulmonary edema.
A good, pleasant and spornic weekend, full of understanding, love and gratitude!
Dorin, Merticaru