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Acute pulmonary edema (APE) is a medical emergency caused by leakage of water from the blood vessels into the lung tissue, making breathing difficult. The edema of the lung has the same pathophysiologic mechanism as any swelling in the body, occurring whenever there is water leakage from blood vessels into a tissue.
Contrary to what one might imagine, our blood vessels tubes are not waterproof, they do have pores that allow the entry and exit of cells, bacteria, proteins and water.
When the left side of the heart becomes weak, it finds it difficult to adequately pump blood to the rest of the body. In heart failure pulmonary edema develops slowly unless there is some factor triggering an acute worsening of heart function. The acute myocardial infarction, commonly known as a heart attack, can be caused by pulmonary edema if there is a large area of the heart muscle on the left side of the heart, leading to sudden heart failure. The increase in pressure tends to be a frequent cause of acute pulmonary edema, especially in patients who already have some degree of heart failure.
In normal situations the patient's heart with moderate heart failure may still be able to pump blood properly. Renal failure leads to accumulation of water and salt in the body, causing an increase in the volume of liquid within the vessels. Some lung infections, particularly those of viral origin, may cause a frame of intense pulmonary inflammation, leading to increased permeability of vessels and subsequent leakage of fluid into the lung. The use of some drugs, such as heroin or cocaine, can cause severe pulmonary inflammation, leading to increased permeability of vessels and subsequent pulmonary edema. Some patients with severe neurological injury, such as head trauma, brain surgery, convulsions, cerebral hemorrhage, etc. Depending on the cause, the picture of pulmonary edema may develop slowly or suddenly, the latter called acute pulmonary edema. In patients accumulating fluid in the lungs slowly and gradually, the symptoms of pulmonary edema begin with intolerance to exertion, fatigue (even at rest), shortness of breath when lying down, no need to use at least two pillows to sleep, swelling in the feet and ankles and wheezing.
If this same patient described above presents a factor of decompensation of their heart failure, such as a heart attack, a hypertensive crisis or even a serious infection, heart suddenly becomes unable to adequately pump blood to the body, and there is a framework of acute fluid retention in the lungs.
The first step in the treatment of acute pulmonary edema is to provide oxygen to the patient.
If the patient does not urinate or does not respond adequately to diuretics, the option is the urgent hemodialysis, a method capable of removing up to a quart of water from the lungs in just 20-30 minutes. 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.
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Use the form below to delete this Dyspnea Is The Cause Cardiac Or Pulmonarya€”or Both Consultant360 image from our index. When the pressure gets too high within the vessels of the lung, water blood tends to "turn into serum" through pores, accumulating within lung tissue, mainly in the alveoli, which are the structures that perform gas exchange. Some diseases, which will be explained below, cause an increase in the pores of blood vessels, making them more permeable, which facilitates the outflow of water. We describe simplified cardiopulmonary circulation for this mechanism so that it is easily understandable. After nourishing all tissues, blood, now low in oxygen and high in carbon dioxide, it returns to the right side of the heart where it is immediately pumped toward the lungs.

As the left side of the heart is responsible for pumping blood from the lungs and when the heart pump fails, there is a jam, causing an accumulation of blood in the pulmonary vessels. If much of the heart muscle dies, the heart becomes unable to pump blood properly, causing this retention in the lungs. However, just a sudden elevation in blood pressure is enough for an increase in resistance to blood flow, requiring further work of the heart muscle. In some cases, especially if the patient does not urinate in appropriate volumes, the quantity of liquid trapped in the vessels becomes so large that it starts to overflow, causing edema and pulmonary edema.
The cause is unknown, but it is believed that there are changes in the pulmonary microvasculature favoring fluid leakage at high altitudes.
This frame is typical in patients with heart failure who have gradual worsening of heart function and progressive pulmonary congestion.
In this case the symptoms of acute pulmonary edema are severe: shortness of breath, feeling of drowning, agitation, cough with frothy secretions, inability to lie down and tachycardia (racing heart). The acute pulmonary edema is a medical emergency and if not treated in time, will definitely lead to cardiac arrest. Usually the patient arrives at the emergency department in hypoxemia, or with low levels of blood oxygenation. 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. Venha conhecer nossa loja pessoalmente ou acesse a pA?gina de produtos e confira alguns dos nossos itens. In the lungs the blood is oxygenated again and returns to the left side of the heart, where it will be pumped into the rest of the body, restarting the process.
This congestion causes an increase in blood pressure in pulmonary vessels, favoring leakage of water. Some patients do not have a heart able to work against high blood pressure, which leads to pulmonary congestion. If the heart valve does not open properly, blood cannot be drained there through, causing congestion. The edema arises from changes in pulmonary hemodynamics, with increased pressure and permeability in the pulmonary vessels.
In some cases pulmonary edema is so severe and oxygenation is so low, that the patient needs to be intubated and connected to a mechanical ventilator to stay alive.
Lowered blood pressure is also important to facilitate the work of the heart, so usually vasodilators are used.

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