STUDY - Technical - New Dacian's Medicine
Dyspnoea
and Pulmonary Edema (2)
Translation Draft
Let's move on with the differential diagnosis of dyspnea, "discussing" diffuse parenchymal lung diseases! This category includes a large number of diseases, ranging from acute pneumonia to chronic disorders such as sarcoidosis and various forms of pneumoconiosis. History, physical examination findings and x-ray abnormalities often provide useful indications for diagnosis. Patients are often tachypneic, with pressure of carbon dioxide and arterial oxygen below normal values. The effort often further reduces the pressure of arterial oxygen. Lung volumes are low, and the lungs are stiff, meaning they have a lower than normal compliance.
We continue with vascular occlusive lung disease. Repeated episodes of dyspnea at rest often occur in recurrent pulmonary embolism. Highlighting a source of embolism, such as phlebitis of the lower extremities or pelvis, is helpful in guiding the doctor to diagnosis. Arterial blood gases are most often abnormal, but lung volumes are frequently normal or abnormalities are minimal.
In the case of diseases of the chest wall or respiratory muscles, the physical examination determines the presence of a disease of the chest wall, such as cyphoscoliosis, excavated thorax or ankylosing spondylitis. Although all this may be associated with dyspnea, only severe cyphoscoliosis constantly interferes with ventilation, enough to produce chronic pulmonary heart and respiratory failure. Both weakness and paralysis of the respiratory muscles can lead to respiratory failure and dyspnoea, but most often the signs and symptoms of neurological or muscle disorders are more important as manifestation in other systems.
In the case of heart disease, in cardiac patients, exercise dyspnea most often occurs as a consequence of increased pulmonary capillary pressure, which in turn may be due to left ventricular dysfunction, reduced left ventricular compliance and mitral stenosis. Increased hydrostatic pressure in the pulmonary vascular bed tends to reverse Starling balance by transwelding the fluid into the interstitial fluid, reducing lung compliance and stimulating J receptors (juxtacapapilari) in the alveolar interstitial space.
Prolonged venous hypertension has the effect of thickening the walls of small pulmonary vessels and an increase in perivascular cells and fibrous tissue, leading to further reduction of compliance. Competition for space between ships, airways and increased fluid in interstitial spaces reduces the lumen of small airways, increasing resistance in the airways. Decrease in compliance and increase resistance to air penetration increases respiratory effort. In severe congestive heart failure, which usually involves both increased pulmonary and systemic venous pressure, hydrothorax can develop, further interfering with lung function and intensifying dyspnea.
Ortopnea, i.e. dyspnea in clinostatism and nocturnal paroxysmal dyspnea, i.e. shortness of breath, which usually occur at night and wake the patient from sleep, characterizes advanced forms of heart failure associated with an increase in venous and pulmonary capillary pressure.
Ortopnea is the result of alteration of the gravitational effect in the lying position that increases venous pressures and pulmonary capillaries. This increase in turn increases the closing lung volume and decreases vital capacity. Paroxysmal (nocturnal) dyspnea, also known as cardiac asthma, is characterized by severe shortness of breath attacks, which usually occur at night and usually wake the patient from sleep. The attack is precipitated by stimuli that aggravate pre-existing pulmonary congestion, frequently, total blood volume being increased at night due to the reabsorption of edema in some parts of the body, during clinostatism.
A sleeping patient can tolerate relatively severe lung load and can only be awakened when true pulmonary edema and bronchospasm have occurred, with the sensation of suffocation and wheezing.
Two other forms of nocturnal dyspnea should be differentiated from that due to heart failure. Chronic bronchitis is characterized by hypersecretion of mucus and, after a few hours of sleep, secretions can accumulate and produce breathlessness and wheezing, both improved by coughing and sputum expectoration. Asthmatic patients have circadian variations in the degree of airway obstruction. The most severe obstruction occurs between 1 and 2 a.m. and may be serious enough for the patient to wake up with a choking sensation, extreme breathlessness and wheezing. Although there is a marked inflammatory component in nocturnal asthma, inhaler bronchodilators usually quickly improve symptoms. In differential diagnosis, Cheyne-Stokes breathing should also be taken into account with everything related to it.
So, the diagnosis of cardiac dyspnea is based on the recognition of heart disease based on clinical examination, supplemented with non-invasive tests. There may be a history of myocardial infarction, cardiac noises three and four may be heard, and/ or left ventricle dilation, distension of the jugular veins in the neck and/ or peripheral edema may be revealed.
Often there are radiological signs of heart failure, with the evidence of interstitial edema, redistribution of pulmonary vascularization and fluid accumulation in the septal areas and in the pleural cavity. Transthoracic ultrasound is particularly useful in establishing the diagnosis of organic heart disease, which may be responsible for dyspnea.
Specifically, dilation of the left atrium and/ or left ventricle, left ventricle hypertrophy, a reduction in the ejection fraction of the left ventricle and motility disorders of the left ventricular wall may be useful clues to support the otherwise unexplained cardiac etiology of dyspnea.
A peculiarity is the differential diagnosis between cardiac and pulmonary dyspnea. In most patients with dyspnea there is clinical evidence of heart and/ or lung disease. Like patients with cardiac dyspnea, those with chronic obstructive pulmonary disease may also wake up at night with dyspnea, but, as mentioned above, it is usually associated with sputum production (dyspnea improves after expectoration).
The difficulty in differentiating cardiac dyspnea from pulmonary dyspnea may be determined by the coexistence of diseases involving both apparatus. It is desirable to carry out lung functionality tests in patients where the etiology of dyspnea is not clear, because these tests may be useful in determining whether dyspnea is caused by heart disease, lung disease, chest wall abnormalities or anxiety.
In addition, compared to the usual investigations used in the evaluation of patients for heart disease, the determination of the ejection fraction at rest and during exertion by ultrasound or radioisotopic ventricularography, is useful in the differential diagnosis of dyspnea. The ejection fraction of the left ventricle is low in left ventricular insufficiency, while the ejection fraction of the right ventricle may be decreased at rest or decreased during exercise in patients with severe lung disease. Both ejection fractions are normal at rest and during exercise in dyspnea due to anxiety or hypochondria.
Careful observation during an exercise test on the treadmill will often help to identify the hypochondriac patient or the one in whom dyspnea is secondary to anxiety. In these circumstances, the patient usually complains of shortness of breath, but it seems that it is done effortlessly or is totally irregular.
I'm going to finish this post about dyspnea by presenting a few things about anxious neurosis. Dyspnea that occurs in the patient with anxious neurosis is a difficult symptom to evaluate. Signs and symptoms of acute and chronic hyperventilation do not serve to differentiate anxious neurosis from other conditions, such as recurrent pulmonary embolism.
Another potential confusion occurs when chest pain and electrocardiographic changes accompany hyperventilation syndrome. When it exists and is attributed to this state, commonly referred to as non-circulatory asthenia, chest pain is sharp, transient, short-lived, with variable locations and electrocardiographic changes are most often observed during repolarization. Frequently, sighed and irregular breathing indicates a psychogenic origin of dyspnea.
That's it for today! Tomorrow I'm going to talk about pulmonary edema...
Let's move on with the differential diagnosis of dyspnea, "discussing" diffuse parenchymal lung diseases! This category includes a large number of diseases, ranging from acute pneumonia to chronic disorders such as sarcoidosis and various forms of pneumoconiosis. History, physical examination findings and x-ray abnormalities often provide useful indications for diagnosis. Patients are often tachypneic, with pressure of carbon dioxide and arterial oxygen below normal values. The effort often further reduces the pressure of arterial oxygen. Lung volumes are low, and the lungs are stiff, meaning they have a lower than normal compliance.
We continue with vascular occlusive lung disease. Repeated episodes of dyspnea at rest often occur in recurrent pulmonary embolism. Highlighting a source of embolism, such as phlebitis of the lower extremities or pelvis, is helpful in guiding the doctor to diagnosis. Arterial blood gases are most often abnormal, but lung volumes are frequently normal or abnormalities are minimal.
In the case of diseases of the chest wall or respiratory muscles, the physical examination determines the presence of a disease of the chest wall, such as cyphoscoliosis, excavated thorax or ankylosing spondylitis. Although all this may be associated with dyspnea, only severe cyphoscoliosis constantly interferes with ventilation, enough to produce chronic pulmonary heart and respiratory failure. Both weakness and paralysis of the respiratory muscles can lead to respiratory failure and dyspnoea, but most often the signs and symptoms of neurological or muscle disorders are more important as manifestation in other systems.
In the case of heart disease, in cardiac patients, exercise dyspnea most often occurs as a consequence of increased pulmonary capillary pressure, which in turn may be due to left ventricular dysfunction, reduced left ventricular compliance and mitral stenosis. Increased hydrostatic pressure in the pulmonary vascular bed tends to reverse Starling balance by transwelding the fluid into the interstitial fluid, reducing lung compliance and stimulating J receptors (juxtacapapilari) in the alveolar interstitial space.
Prolonged venous hypertension has the effect of thickening the walls of small pulmonary vessels and an increase in perivascular cells and fibrous tissue, leading to further reduction of compliance. Competition for space between ships, airways and increased fluid in interstitial spaces reduces the lumen of small airways, increasing resistance in the airways. Decrease in compliance and increase resistance to air penetration increases respiratory effort. In severe congestive heart failure, which usually involves both increased pulmonary and systemic venous pressure, hydrothorax can develop, further interfering with lung function and intensifying dyspnea.
Ortopnea, i.e. dyspnea in clinostatism and nocturnal paroxysmal dyspnea, i.e. shortness of breath, which usually occur at night and wake the patient from sleep, characterizes advanced forms of heart failure associated with an increase in venous and pulmonary capillary pressure.
Ortopnea is the result of alteration of the gravitational effect in the lying position that increases venous pressures and pulmonary capillaries. This increase in turn increases the closing lung volume and decreases vital capacity. Paroxysmal (nocturnal) dyspnea, also known as cardiac asthma, is characterized by severe shortness of breath attacks, which usually occur at night and usually wake the patient from sleep. The attack is precipitated by stimuli that aggravate pre-existing pulmonary congestion, frequently, total blood volume being increased at night due to the reabsorption of edema in some parts of the body, during clinostatism.
A sleeping patient can tolerate relatively severe lung load and can only be awakened when true pulmonary edema and bronchospasm have occurred, with the sensation of suffocation and wheezing.
Two other forms of nocturnal dyspnea should be differentiated from that due to heart failure. Chronic bronchitis is characterized by hypersecretion of mucus and, after a few hours of sleep, secretions can accumulate and produce breathlessness and wheezing, both improved by coughing and sputum expectoration. Asthmatic patients have circadian variations in the degree of airway obstruction. The most severe obstruction occurs between 1 and 2 a.m. and may be serious enough for the patient to wake up with a choking sensation, extreme breathlessness and wheezing. Although there is a marked inflammatory component in nocturnal asthma, inhaler bronchodilators usually quickly improve symptoms. In differential diagnosis, Cheyne-Stokes breathing should also be taken into account with everything related to it.
So, the diagnosis of cardiac dyspnea is based on the recognition of heart disease based on clinical examination, supplemented with non-invasive tests. There may be a history of myocardial infarction, cardiac noises three and four may be heard, and/ or left ventricle dilation, distension of the jugular veins in the neck and/ or peripheral edema may be revealed.
Often there are radiological signs of heart failure, with the evidence of interstitial edema, redistribution of pulmonary vascularization and fluid accumulation in the septal areas and in the pleural cavity. Transthoracic ultrasound is particularly useful in establishing the diagnosis of organic heart disease, which may be responsible for dyspnea.
Specifically, dilation of the left atrium and/ or left ventricle, left ventricle hypertrophy, a reduction in the ejection fraction of the left ventricle and motility disorders of the left ventricular wall may be useful clues to support the otherwise unexplained cardiac etiology of dyspnea.
A peculiarity is the differential diagnosis between cardiac and pulmonary dyspnea. In most patients with dyspnea there is clinical evidence of heart and/ or lung disease. Like patients with cardiac dyspnea, those with chronic obstructive pulmonary disease may also wake up at night with dyspnea, but, as mentioned above, it is usually associated with sputum production (dyspnea improves after expectoration).
The difficulty in differentiating cardiac dyspnea from pulmonary dyspnea may be determined by the coexistence of diseases involving both apparatus. It is desirable to carry out lung functionality tests in patients where the etiology of dyspnea is not clear, because these tests may be useful in determining whether dyspnea is caused by heart disease, lung disease, chest wall abnormalities or anxiety.
In addition, compared to the usual investigations used in the evaluation of patients for heart disease, the determination of the ejection fraction at rest and during exertion by ultrasound or radioisotopic ventricularography, is useful in the differential diagnosis of dyspnea. The ejection fraction of the left ventricle is low in left ventricular insufficiency, while the ejection fraction of the right ventricle may be decreased at rest or decreased during exercise in patients with severe lung disease. Both ejection fractions are normal at rest and during exercise in dyspnea due to anxiety or hypochondria.
Careful observation during an exercise test on the treadmill will often help to identify the hypochondriac patient or the one in whom dyspnea is secondary to anxiety. In these circumstances, the patient usually complains of shortness of breath, but it seems that it is done effortlessly or is totally irregular.
I'm going to finish this post about dyspnea by presenting a few things about anxious neurosis. Dyspnea that occurs in the patient with anxious neurosis is a difficult symptom to evaluate. Signs and symptoms of acute and chronic hyperventilation do not serve to differentiate anxious neurosis from other conditions, such as recurrent pulmonary embolism.
Another potential confusion occurs when chest pain and electrocardiographic changes accompany hyperventilation syndrome. When it exists and is attributed to this state, commonly referred to as non-circulatory asthenia, chest pain is sharp, transient, short-lived, with variable locations and electrocardiographic changes are most often observed during repolarization. Frequently, sighed and irregular breathing indicates a psychogenic origin of dyspnea.
That's it for today! Tomorrow I'm going to talk about pulmonary edema...
A Sunday of the best, full
of understanding, love and gratitude!
Dorin, Merticaru