Causes of edema due to increased capillary pressure queen,survival food south africa,fort edmonton park 2015 - Plans On 2016

All content on this website, including dictionary, thesaurus, literature, geography, and other reference data is for informational purposes only. Acute pulmonary edema is a pathological condition defined by the presence of large amounts of fluid in pulmonary alveoli and in pulmonary interstitium. Cardiogenic acute pulmonary edema by decreasing blood evacuation from the left atrium: atrial fibrillation, acute mitral regurgitation, mitral stenosis, thrombus or myxoma in the left atrium.
Cardiogenic acute pulmonary edema caused by left ventricular diastolic dysfunction: aortic stenosis, hypertension, hypertrophic cardiomyopathy, acute myocardial ischemia. Cardiogenic acute pulmonary edema caused by left ventricular systolic dysfunction: acute myocardial ischemia, myocarditis, dilated cardiomyopathy, heart failure. Increased capillary permeability (acute respiratory distress syndrome): pneumonia, aspiration syndrome, inhalation of toxic gases, disseminated intravascular coagulation, anaphylaxis shock, acute pancreatitis. Incompletely understood causes: altitude acute pulmonary edema, neurogenic acute pulmonary edema, eclamsie, post anesthesia and post cardio-conversion. Cardiogenic acute pulmonary edema is caused due to the increase pulmonary capillary pressure from 8-12 mm Hg (normal) to over 18 mm Hg. The main symptoms of acute pulmonary edema are the shortness of breath, cough, marked anxiety, cold and increased sweating and symptoms of the background heart disease.
Dyspnea is very intense, may occur in a patient who had until then no charge of this symptom (for example, a acute pulmonary edema that occurs after the onset of a myocardial infarction), or can overlap with the symptoms of preexisting heart failure . A patient that is restless, anxious or confused with sweaty, pale or mottled skin, with central type cyanosis, the patient is breathing typically standing at the edge of the bed and using accessory respiratory muscles. Marked dyspnea, possibly vesicular murmur and prolonged expiration, rales crackles, of which level increases from the bases of the lungs to tops and can include the entire lung field. Tachycardia, hypertension or hypotension and, depending on the case, rhythm disturbances or different heart murmurs. In some cases, may appear signs of right heart failure: hepatomegaly, jugular turgor, hepato-jugular reflux, lower limb edema.
Echocardiography can detect the presence of valvulopathies, of thrombus or myxoma in the left atrium, impaired function of the left ventricle. Positive diagnosis of cardiogenic acute pulmonary edema is relatively simple, it is based on patient history and symptoms.



General measures: keep the patient in a sitting position, administration of oxygen on mask or nasal tube, dyspnea sedation with morphine. Furosemide, administrated intravenous in dose of 80-120 mg or more, divided into four doses of 40 mg, each, is the primary mean of treatment of cardiogenic acute pulmonary edema.
Nitroglycerin, vasodilator with rapid effect, administrated sublingual (0.5 mg tablets, the dose can be repeated in 5-10 minutes) or intravenously, in the conditions of systolic blood pressure higher than 100 mm Hg. Administration of digoxin can bring benefits by improving the cardiac tonus or by decreasing the heart rate in case of atrial fibrillation. Other therapeutic measures in cardiogenic acute pulmonary edema are: miofilin administration or the administration of angiotensin converting enzyme inhibitors, assisted ventilation, circulatory support with counterpulsation balloon and the treatment of the cause that led to the installation of cardiogenic acute pulmonary edema. Tell a friend about us, add a link to this page, or visit the webmaster's page for free fun content.
Cardiogenic acute pulmonary edema is an acute form of heart failure caused by increased pressure in the pulmonary capillary. In severe forms may be present hypercapnia and respiratory acidosis, which constitute signs of gravity. Its beneficial effects are explained by the occurrence of venous dilation, which will lead to decreased preload (quickly installed) and diuresis (which occurs in 20-90 minutes after the administration of furosemide). Digoxin administration is contraindicated in cardiogenic acute pulmonary edema associated with mitral stenosis or with acute myocardial infarction.
This accumulation can occur in the cells (cellular edema), in the intercellular spaces within tissues (interstitial edema), or in potential spaces within the body. Edema may also be classified by location, such as pulmonary edema or brain edema; types found in certain locations have specific names, such as ascites (peritoneal cavity), hydrothorax (pleural cavity), or hydropericardium (pericardial sac). Classification by location does not indicate whether the edema is cellular or interstitial or occupies a potential space (for example, brain edema may be either cellular or interstitial). Edema can be caused by a variety of factors, including conditions that affect osmotic pressure, such as hypotonic fluid overload, which allows the movement of water into the intracellular space, or hypoproteinemia, which decreases the concentration of plasma proteins and permits the passage of fluid out of the blood vessels into the tissue spaces. With trauma, increased capillary permeability and dilation cause leaking into tissue space. Initially clear, exudate in the tissue space becomes more viscous with an increase in plasma protein.


This may occur because of decreased osmolality of the fluid surrounding the cells, as in hypotonic fluid overload, or increased osmolality of the intracellular fluid, as in conditions that decrease the activity of the sodium pump of the cell membrane, allowing the concentration of sodium ions within the cell to increase.cerebral edema swelling of the brain caused by the accumulation of fluid in the brain substance.
It may result from head injury, stroke, infection, hypoxia, brain tumors, obstructive hydrocephalus, and lead encephalopathy; it may also be caused by disturbances in fluid and electrolyte balance that accompany hemodialysis and diabetic ketoacidosis.
The most common type is vasogenic edema, which may result from increased capillary pressure or from increased capillary permeability caused by trauma to the capillary walls. Because the brain is enclosed in the solid vault of the skull, edema compresses the blood vessels, decreasing the blood flow and causing ischemia and hypoxia, which in turn result in further edema.
See also nonpitting edema.pulmonary edema diffuse extravascular accumulation of fluid in the tissues and air spaces of the lung due to changes in hydrostatic forces in the capillaries or to increased capillary permeability. It is most often symptomatic of left ventricular heart failure, but can also be a complication of mitral stenosis, aortic stenosis, altitude sickness, acute hypertension, volume overload during intravenous therapy, or reduced serum oncotic pressure, as in patients who have nephrosis, cirrhosis, or hypoalbuminemia.During the initial stage of pulmonary edema, patients may complain of restlessness and anxiety and the feeling that they are getting a common cold. As fluid continues to fill the pulmonary interstitial spaces the dyspnea becomes more acute, respirations increase in rate, and there is audible wheezing. Eventually, if the condition persists, the patient becomes less responsive to stimuli as levels of consciousness decrease.
In some patients these phases are telescoped as the pulmonary edema develops rapidly and the final stages of respiratory insufficiency are evident in a very short period of time.Treatment is aimed at enhancing gas exchange, reducing fluid overload, and strengthening and slowing the heart beat. To accomplish these goals the patient is often given oxygen by mask or through mechanically assisted ventilation. Drug therapy includes diuretics to remove excess alveolar fluid and morphine to relieve anxiety and reduce the effort of breathing.
The cause is usually the movement of blood components through the pulmonary capillary walls as a result of a change in osmotic pressure, an increased permeability of the walls, or related factors.



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