STUDY - Technical - New Dacian's Medicine
Dyspnoea
and Pulmonary Edema (3)
Translation Draft
Pulmonary edema is most commonly classified on the basis of the initiation mechanism, based on the considerations about 1. Starling force imbalance, 2. alteration of the permeability of the alveolo-capillary membrane (adult respiratory distress syndrome), 3. lymphatic failure and 4. other unknown or incompletely understood mechanisms.
Detailing, starling force imbalance is manifested due to: 1. increased pulmonary capillary pressure: a. increased pulmonary venous pressure without left ventricular insufficiency (e.g. mitral stenosis), b. increased pulmonary venous pressure, secondary to left ventricular insufficiency and c. increased pulmonary capillary pressure, secondary to increased pulmonary arterial pressure (so-called hyperperfusion pulmonary edema), 2. low plasma oncotic pressure, mainly due to hypoalbuminemia, and 3. increase in the negativity of interstitial pressure due to a. rapid development of pneumothorax with the appearance of high negative pressures (unilateral) and b. high negative pleural pressures due to acute airway obstruction with increased final exhaling volume (asthma).
In case of alteration of the permeability of the alveolo-capillary membrane there are several determinisms represented by 1. infectious pneumonia (bacterial, viral, parasitic), 2. inhaled toxins (e.g. phosgen, ozone, chlorides, industrial noxes, nitrogen dioxide, cigarette smoke), 3. circulating foreign substances (e.g. snake venom, bacterial endotoxins), 4. aspiration of acidic gastric contents, 5. acute irradiation pneumonia, 6. endogenous vasoactive substances (e.g. histamine, kinin), 7. disseminated intravascular coagulation, 8. immuno-allergic pneumonitis, medicines (nitrofurantoin) and leukoaglutinin, 9. "shock lung" in combination with nonthoracic trauma and 10. acute hemorrhagic pancreatitis.
In the case of lymphatic failure we have the following determinisms: 1. after lung transplantation, 2. lymphangitic carcinomatosis and 3. fibrous lymphangitis (e.g. silicosis). For unknown or incomplete mechanisms, the following shall be defined: 1. high-altitude pulmonary edema and 2. neurogenic, 3. narcotics overdose, 4. pulmonary embolism, 5. eclampsia, 6. associated with cardioversion, 7. associated with anesthesia and 8. after cardiopulmonary bypass.
I will first present some elements related to cardiogenic pulmonary edema. An increase in pulmonary venous pressure, which initially causes the loading of pulmonary vascularization, is common in most cases of dyspnea in association with congestive heart failure.
Lungs become less compliant, increase resistance in the small airways and there is an increase in lymphatic flow, which apparently serves to maintain constant volume of extravascular pulmonary fluid. A medium tachypnea is present. if it is sufficient both in size and duration, the increase in intravascular pressure leads to a net gain of fluid in the extravascular space, i.e. interstitial edema is installed. At this point, symptoms worsen, tachypnea increases, gas exchange deteriorates further and radiological changes occur, such as Kerley B lines and removal of vascular lines.
At this stage, the intercellular junctions of the capillary endothelium are enlarged and allow macromolecules to pass into the interstitial. An even greater increase in intravascular pressure causes the tight junctions between the cells of the alveolar basal membrane to break and the alveolar edema occurs through the leakage of fluid containing hematia and macromolecules. At this time alveolar edema is present.
By more severe insults of the alveolo-capillary membrane, the edematos fluid floods the alveoli and airways. At this time, clinically expressed pulmonary edema occurs, with bilateral wet rals and ronhuss, and thoracic X-rays may show diffuse veiling of pulmonary fields with higher density proximal to the hilarious regions.
Characteristic is that the patient is anxious and sweats profusely, and the sputum is foamy and pinkish. Gas exchange is affected even more severely, with worsening hypoxia. Without effective treatment, acidicemia, hypercapnia and stopping breathing are progressively established.
It's the turn of noncardiogenic pulmonary edema. A number of clinical situations are associated with pulmonary edema installed by the imbalance between Starling forces, other than that caused by the primary increase in pulmonary capillary pressure. Although we can expect that the decreased oncotic pressure of plasma in hypoalbuminemia states (e.g. severe liver disease, nephrotic syndrome, enteropathy with loss of protein), will lead to pulmonary edema, the balance of forces normally strongly favors resorption, so that even in these conditions an increase in capillary pressure is usually required before the appearance of interstitial edema.
Increased negativity of interstitial pressure was involved in the genesis of unilateral pulmonary edema after the rapid evacuation of a massive pneumothorax. In this situation, the changes may be obvious only radiologically, but the patient occasionally experiences dyspnoea, with objective physical signs localized in the edematos lung.
It has been suggested that the significant negative intrapleural pressure that occurs in severe asthma may be associated with the development of interstitial edema. Lymphatic blockage secondary to inflammatory and fibrous diseases or carcinomatous lymphangitis can cause interstitial edema. In such situations, both clinical and radiological manifestations are dominated by those of the underlying disease.
Other situations characterized by increased interstitial fluid in the lungs seem to be associated from the beginning with damage to the alveolo-capillary membrane. Any toxic aggression that occurs spontaneously or is present in the environment, including diffuse pulmonary infections, aspiration and shock (in particular that due to septicaemia and hemorrhagic pancreatitis and after cardiopulmonary bypass) is associated with diffuse pulmonary edema, which clearly does not have a hemodynamic origin. These situations can lead to respiratory distress syndrome.
There are other forms of pulmonary edema, represented by three forms of pulmonary edema that were not clearly related to increased permeability, inadequate lymph flow or imbalance of Starling forces (for this reason their precise mechanism is not explained). Overdose of narcotics often occurs in the history of pulmonary edema.
Although the illicit use of parenteral heroin is the most common cause, parenteral and oral overdose of preparations related to morphine, methadone and dextropropoxyfen has been associated with pulmonary edema.
The explanation so far that injected impurities cause the disorder is no longer allowed. Available evidence suggests that there are alterations in the permeability of the alveolar membrane and capillaries, rather than increases in capillary pulmonary pressure. Exposure to high altitude in combination with high physical exertion is recognized as a factor that can promote pulmonary edema in unacclimatized people, even healthy people.
Recent data show that natives acclimatized at high altitudes also develop this syndrome when they return to high altitudes after a short period spent at low altitudes. The syndrome is more common in people under 25 years of age. The mechanism involved in the production of pulmonary edema at high altitudes remains unknown, and the results of the studies carried out are controversial, some indicating pulmonary venous constriction, others pulmonary arteriolar constriction, as the primary mechanism.
A role of high-altitude hypoxia is suggested by patients responding to oxygen administration and/ or return to lower altitudes. Hypoxia itself does not alter the permeability of the alveolo-capillary membrane. Therefore, increased heart rate and pulmonary arterial pressure during physical exertion, combined with hypoxic pulmonary arteriolar constriction, which is more pronounced in young people, may coexist, this being an example of high-pressure prearteriolar pulmonary edema.
Neurogenic pulmonary edema has been described in patients with central nervous system diseases and no previously known left ventricle dysfunction. Although most experimental evidence involved the activity of the sympathetic nervous system, the mechanism by which sympathetic efferent activity leads to pulmonary edema is pure speculation. It is known that a massive adrenergic discharge leads to peripheral vasoconstriction, with increased blood pressure and blood sending into the central circulation.
In addition, there is probably a reduction in the compliance of the left ventricle, both factors serving to increase the left atrial pressure long enough to produce pulmonary edema by hemodynamic mechanism. Some experimental evidence suggests that stimulation of adrenergic receptors directly increases capillary permeability, but this effect is relatively minor compared to the imbalance of Starling forces.
From tomorrow we'll move on to coughing and hemoptysis...
Pulmonary edema is most commonly classified on the basis of the initiation mechanism, based on the considerations about 1. Starling force imbalance, 2. alteration of the permeability of the alveolo-capillary membrane (adult respiratory distress syndrome), 3. lymphatic failure and 4. other unknown or incompletely understood mechanisms.
Detailing, starling force imbalance is manifested due to: 1. increased pulmonary capillary pressure: a. increased pulmonary venous pressure without left ventricular insufficiency (e.g. mitral stenosis), b. increased pulmonary venous pressure, secondary to left ventricular insufficiency and c. increased pulmonary capillary pressure, secondary to increased pulmonary arterial pressure (so-called hyperperfusion pulmonary edema), 2. low plasma oncotic pressure, mainly due to hypoalbuminemia, and 3. increase in the negativity of interstitial pressure due to a. rapid development of pneumothorax with the appearance of high negative pressures (unilateral) and b. high negative pleural pressures due to acute airway obstruction with increased final exhaling volume (asthma).
In case of alteration of the permeability of the alveolo-capillary membrane there are several determinisms represented by 1. infectious pneumonia (bacterial, viral, parasitic), 2. inhaled toxins (e.g. phosgen, ozone, chlorides, industrial noxes, nitrogen dioxide, cigarette smoke), 3. circulating foreign substances (e.g. snake venom, bacterial endotoxins), 4. aspiration of acidic gastric contents, 5. acute irradiation pneumonia, 6. endogenous vasoactive substances (e.g. histamine, kinin), 7. disseminated intravascular coagulation, 8. immuno-allergic pneumonitis, medicines (nitrofurantoin) and leukoaglutinin, 9. "shock lung" in combination with nonthoracic trauma and 10. acute hemorrhagic pancreatitis.
In the case of lymphatic failure we have the following determinisms: 1. after lung transplantation, 2. lymphangitic carcinomatosis and 3. fibrous lymphangitis (e.g. silicosis). For unknown or incomplete mechanisms, the following shall be defined: 1. high-altitude pulmonary edema and 2. neurogenic, 3. narcotics overdose, 4. pulmonary embolism, 5. eclampsia, 6. associated with cardioversion, 7. associated with anesthesia and 8. after cardiopulmonary bypass.
I will first present some elements related to cardiogenic pulmonary edema. An increase in pulmonary venous pressure, which initially causes the loading of pulmonary vascularization, is common in most cases of dyspnea in association with congestive heart failure.
Lungs become less compliant, increase resistance in the small airways and there is an increase in lymphatic flow, which apparently serves to maintain constant volume of extravascular pulmonary fluid. A medium tachypnea is present. if it is sufficient both in size and duration, the increase in intravascular pressure leads to a net gain of fluid in the extravascular space, i.e. interstitial edema is installed. At this point, symptoms worsen, tachypnea increases, gas exchange deteriorates further and radiological changes occur, such as Kerley B lines and removal of vascular lines.
At this stage, the intercellular junctions of the capillary endothelium are enlarged and allow macromolecules to pass into the interstitial. An even greater increase in intravascular pressure causes the tight junctions between the cells of the alveolar basal membrane to break and the alveolar edema occurs through the leakage of fluid containing hematia and macromolecules. At this time alveolar edema is present.
By more severe insults of the alveolo-capillary membrane, the edematos fluid floods the alveoli and airways. At this time, clinically expressed pulmonary edema occurs, with bilateral wet rals and ronhuss, and thoracic X-rays may show diffuse veiling of pulmonary fields with higher density proximal to the hilarious regions.
Characteristic is that the patient is anxious and sweats profusely, and the sputum is foamy and pinkish. Gas exchange is affected even more severely, with worsening hypoxia. Without effective treatment, acidicemia, hypercapnia and stopping breathing are progressively established.
It's the turn of noncardiogenic pulmonary edema. A number of clinical situations are associated with pulmonary edema installed by the imbalance between Starling forces, other than that caused by the primary increase in pulmonary capillary pressure. Although we can expect that the decreased oncotic pressure of plasma in hypoalbuminemia states (e.g. severe liver disease, nephrotic syndrome, enteropathy with loss of protein), will lead to pulmonary edema, the balance of forces normally strongly favors resorption, so that even in these conditions an increase in capillary pressure is usually required before the appearance of interstitial edema.
Increased negativity of interstitial pressure was involved in the genesis of unilateral pulmonary edema after the rapid evacuation of a massive pneumothorax. In this situation, the changes may be obvious only radiologically, but the patient occasionally experiences dyspnoea, with objective physical signs localized in the edematos lung.
It has been suggested that the significant negative intrapleural pressure that occurs in severe asthma may be associated with the development of interstitial edema. Lymphatic blockage secondary to inflammatory and fibrous diseases or carcinomatous lymphangitis can cause interstitial edema. In such situations, both clinical and radiological manifestations are dominated by those of the underlying disease.
Other situations characterized by increased interstitial fluid in the lungs seem to be associated from the beginning with damage to the alveolo-capillary membrane. Any toxic aggression that occurs spontaneously or is present in the environment, including diffuse pulmonary infections, aspiration and shock (in particular that due to septicaemia and hemorrhagic pancreatitis and after cardiopulmonary bypass) is associated with diffuse pulmonary edema, which clearly does not have a hemodynamic origin. These situations can lead to respiratory distress syndrome.
There are other forms of pulmonary edema, represented by three forms of pulmonary edema that were not clearly related to increased permeability, inadequate lymph flow or imbalance of Starling forces (for this reason their precise mechanism is not explained). Overdose of narcotics often occurs in the history of pulmonary edema.
Although the illicit use of parenteral heroin is the most common cause, parenteral and oral overdose of preparations related to morphine, methadone and dextropropoxyfen has been associated with pulmonary edema.
The explanation so far that injected impurities cause the disorder is no longer allowed. Available evidence suggests that there are alterations in the permeability of the alveolar membrane and capillaries, rather than increases in capillary pulmonary pressure. Exposure to high altitude in combination with high physical exertion is recognized as a factor that can promote pulmonary edema in unacclimatized people, even healthy people.
Recent data show that natives acclimatized at high altitudes also develop this syndrome when they return to high altitudes after a short period spent at low altitudes. The syndrome is more common in people under 25 years of age. The mechanism involved in the production of pulmonary edema at high altitudes remains unknown, and the results of the studies carried out are controversial, some indicating pulmonary venous constriction, others pulmonary arteriolar constriction, as the primary mechanism.
A role of high-altitude hypoxia is suggested by patients responding to oxygen administration and/ or return to lower altitudes. Hypoxia itself does not alter the permeability of the alveolo-capillary membrane. Therefore, increased heart rate and pulmonary arterial pressure during physical exertion, combined with hypoxic pulmonary arteriolar constriction, which is more pronounced in young people, may coexist, this being an example of high-pressure prearteriolar pulmonary edema.
Neurogenic pulmonary edema has been described in patients with central nervous system diseases and no previously known left ventricle dysfunction. Although most experimental evidence involved the activity of the sympathetic nervous system, the mechanism by which sympathetic efferent activity leads to pulmonary edema is pure speculation. It is known that a massive adrenergic discharge leads to peripheral vasoconstriction, with increased blood pressure and blood sending into the central circulation.
In addition, there is probably a reduction in the compliance of the left ventricle, both factors serving to increase the left atrial pressure long enough to produce pulmonary edema by hemodynamic mechanism. Some experimental evidence suggests that stimulation of adrenergic receptors directly increases capillary permeability, but this effect is relatively minor compared to the imbalance of Starling forces.
From tomorrow we'll move on to coughing and hemoptysis...
One of the best weeks!
Dorin, Merticaru