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Oedema Neurogenic Pulmonary

Zhabrov
15.06.2018

Content:

  • Oedema Neurogenic Pulmonary
  • Pulmonary edema
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  • Neurogenic pulmonary edema (NPE) is a relatively rare form of pulmonary edema caused by an increase in pulmonary interstitial and alveolar. Neurogenic pulmonary edema (NPE) is a clinical syndrome characterized by the acute onset of pulmonary edema following a significant. Neurogenic pulmonary edema (NPE) is an increase in pulmonary interstitial and alveolar fluid that is due to an acute central nervous system.

    Oedema Neurogenic Pulmonary

    The lower chambers the more muscular right and left ventricles pump blood out of your heart. The heart valves — which keep blood flowing in the correct direction — are gates at the chamber openings. Normally, deoxygenated blood from all over your body enters the right atrium and flows into the right ventricle, where it's pumped through large blood vessels pulmonary arteries to your lungs. There, the blood releases carbon dioxide and picks up oxygen.

    The oxygen-rich blood then returns to the left atrium through the pulmonary veins, flows through the mitral valve into the left ventricle and finally leaves your heart through another large artery, the aorta.

    The aortic valve at the base of the aorta keeps the blood from flowing backward into your heart. From the aorta, the blood travels to the rest of your body. Cardiogenic pulmonary edema is a type of pulmonary edema caused by increased pressures in the heart. This condition usually occurs when the diseased or overworked left ventricle isn't able to pump out enough of the blood it receives from your lungs congestive heart failure. As a result, pressure increases inside the left atrium and then in the veins and capillaries in your lungs, causing fluid to be pushed through the capillary walls into the air sacs.

    Over time, the arteries that supply blood to your heart muscle can become narrow from fatty deposits plaques. A heart attack occurs when a blood clot forms in one of these narrowed arteries, blocking blood flow and damaging the portion of your heart muscle supplied by that artery. The result is that the damaged heart muscle can no longer pump as well as it should. Sometimes, a clot isn't the cause of the problem.

    Instead, gradual narrowing of the coronary arteries can lead to weakness of the left ventricular muscle. Although the rest of your heart tries to compensate for this loss, there are times when it's unable to do so effectively. The heart can also be weakened by the extra workload. When the pumping action of your heart is weakened, blood gradually backs up into your lungs, forcing fluid in your blood to pass through the capillary walls into the air sacs.

    This is chronic congestive heart failure. In mitral valve disease or aortic valve disease, the valves that regulate blood flow in the left side of your heart may not open wide enough stenosis. Or, they don't close completely, allowing blood to flow backward through the valve insufficiency or regurgitation. When the valves are narrowed, blood can't flow freely into your heart and pressure in the left ventricle builds up, causing the left ventricle to work harder and harder with each contraction.

    The left ventricle also dilates to allow greater blood flow, but this makes the left ventricle's pumping action less efficient. The increased pressure extends into the left atrium and then to the pulmonary veins, causing fluid to accumulate in your lungs. On the other hand, if the mitral valve leaks, some blood is backwashed toward your lung each time your heart pumps. If the leakage develops suddenly, you may develop sudden and severe pulmonary edema.

    Other conditions may lead to cardiogenic pulmonary edema, such as high blood pressure due to narrowed kidney arteries renal artery stenosis and fluid buildup due to kidney disease or heart problems. In normal lungs, air sacs alveoli take in oxygen and release carbon dioxide. In high-altitude pulmonary edema HAPE , it's theorized that vessels in the lungs constrict, causing increased pressure. This causes fluid to leak from the blood vessels to the lung tissues and eventually into the air sacs.

    Pulmonary edema that isn't caused by increased pressures in your heart is called noncardiogenic pulmonary edema. In this condition, fluid may leak from the capillaries in your lungs' air sacs because the capillaries themselves become more permeable or leaky, even without the buildup of back pressure from your heart.

    Some factors that can cause noncardiogenic pulmonary edema include:. Mountain climbers and people who travel to high-altitude locations run the risk of developing high-altitude pulmonary edema HAPE. This condition — which generally occurs at elevations above 8, feet about 2, meters — can also affect hikers or skiers who start exercising at higher altitudes without first becoming acclimated, which can take from a few days to a week or so.

    But even people who have hiked or skied at high altitudes in the past aren't immune. Although the exact cause isn't completely understood, HAPE seems to develop as a result of increased pressure from constriction of the pulmonary capillaries. Without appropriate care, HAPE can be fatal, but this risk can be minimized. If pulmonary edema continues, it can raise pressure in the pulmonary artery pulmonary hypertension , and eventually the right ventricle in your heart becomes weak and begins to fail.

    The right ventricle has a much thinner wall of muscle than does the left side of your heart because it is under less pressure to pump blood into the lungs. The increased pressure backs up into the right atrium and then into various parts of your body, where it can cause:.

    Left untreated, acute pulmonary edema can be deadly. In some instances, it may be fatal even if you receive treatment. Preventing conditions and situations that cause pulmonary edema can help keep pulmonary edema from developing. These measures can help reduce your risk. Cardiovascular disease is the leading cause of pulmonary edema. You can reduce your risk of many kinds of heart problems by following these suggestions:.

    Watch your blood cholesterol. Cholesterol is one of several types of fats essential to good health. But too much cholesterol can be too much of a good thing. Higher than normal cholesterol levels can cause fatty deposits to form in your arteries, impeding blood flow and increasing your risk of vascular disease. But lifestyle changes can often keep your cholesterol levels low.

    Lifestyle changes may include limiting fats especially saturated fats ; eating more fiber, fish, and fresh fruits and vegetables; exercising regularly; stopping smoking; and drinking in moderation.

    It's especially important to use less salt sodium if you have heart disease or high blood pressure. In some people with severely damaged left ventricular function, excess salt may be enough to trigger congestive heart failure.

    If you're having a hard time cutting back on salt, it may help to talk to a dietitian. He or she can help point out low-sodium foods as well as offer tips for making a low-salt diet interesting and good tasting. If you travel or climb at high altitudes, acclimate yourself slowly. Although recommendations vary, most experts advise ascending no more than 1, to 1, feet about to meters a day once you reach 8, feet about 2, meters. Some climbers take prescription medications such as acetazolamide or nifedipine Procardia to help prevent signs and symptoms of HAPE.

    To prevent HAPE, start taking the medication at least one day before ascent. Continue taking the medication for about five days after you've arrived at your high-altitude destination. Pulmonary edema was diagnosed if the patient had clinical and radiological features of pulmonary edema and arterial hypoxemia arterial oxygen saturation measured while the patient was breathing room air if possible. In patients receiving mechanical ventilation, arterial hypoxemia was defined as present when the ratio of Pa o 2 to the fraction of inspired oxygen was less than The medical committee took particularly into account the presence of signs of respiratory distress cyanosis, inspiratory retraction of intercostal spaces and the presence of lung crackles on auscultation of one or both lungs.

    Manifestations of interstitial pulmonary edema on radiographs included the loss of the normal sharp definition of pulmonary vascular markings, haziness, loss of demarcation of hilar shadows, thickening of interlobular septa, and peribronchial cuffing.

    Radiographic manifestations of alveolar pulmonary edema included unilateral or bilateral confluent acinar shadows creating irregular patchy increases in parenchymal density in the lower two thirds of the lung. In all patients included, cardiac function was explored.

    In 3 patients, left ventricular ejection fraction LVEF was measured by means of echocardiography as soon as feasible within 24 hours after ICU admission. In addition, in 3 patients, the measurements of pulmonary artery wedge pressure, cardiac index, stroke volume index, and systemic vascular resistance were obtained by using a pulmonary artery catheter inserted a few hours after admission to the ICU. In 2 patients, myocardial echocardiography was repeated.

    During the study period, patients were admitted with traumatic head injury. Only 7 patients were finally included in this study. The mean time between traumatic head injury and ICU admission was 1 hour. The traumatic head injury was caused by a traffic accident in all cases. All 7 patients had hyperpnea and tachycardia at the time of hospital admission.

    Cardiogenic shock developed in 1 patient patient 5, treated with dobutamine and norepinephrine on hospital admission. The mean GCS score was 6 range 3— All patients had already received mechanical ventilation before the ICU admission. All 7 patients had clinical manifestations of respiratory distress at the scene of the accident. Demographic and clinical parameters of the study population at admission. All patients had brain CT upon admission. Computed tomography scan of cerebrum of patient 6 shows a subdural hematoma, meningeal hemorrhage, cerebral edema, cerebral contusion, and a pneumocephalus.

    Computed tomography scan of the chest of patient 5 obtained on admission to the intensive care unit shows alveolar pulmonary edema. Echocardiographic studies in 3 patients showed global hypokinesia with a decrease in LVEF to 0.

    In 1 patient patient 4 , however, a diastolic dysfunction with a reduced velocity of early filling E wave , an increase in the velocity associated with atrial contraction A wave , and a ratio of E to A of less than 1 was observed. For 2 patients patients 2 and 6 , echocardiography performed 7 and 90 days after the initial study showed complete recovery, with an LVEF of 0. The electrocardiograms showed some abnormalities in all patients.

    Other abnormalities also were observed, including ST-segment depression in 1 patient and right bundle branch block in 2 patients. Pulmonary artery catheterization was done for 3 patients patients 1, 3, and 7. The findings indicated a low stroke volume index in all 3 patients.

    Pulmonary artery wedge pressure was higher in all patients except patient 3. Postmortem myocardial biopsies were done in 4 cases patients 1, 4, 5, and 7 , and a pulmonary biopsy was done in 1 case patient 5. Myocardial biopsy showed an interstitial edema in all cases without a focus of necrotic muscle fiber or myocardial infiltration by inflammatory cells. Photomicrograph of histological examination of myocardial biopsy specimen from patient 5 shows interstitial myocardial edema arrows with no myocyte injury and inflammatory infiltrate hematoxylineosin, original magnification x Photomicrograph of histological examination of pulmonary biopsy specimen from patient 5 shows uniform edematous change in the alveolar septa with dilated lymphatic channels, accumulation of red blood cells, and intraalveolar edema hematoxylineosin, original magnification x In all patients included in the study, the diagnosis of cardiac dysfunction was suspected because of the signs of acute respiratory distress cyanosis, inspiratory retraction of intercostal spaces , the presence of crackles on auscultation of one or both lungs, and the evidence of pulmonary edema on the chest radiograph.

    In patients who underwent echocardiography, the cardiogenic part was confirmed by a low LVEF at 0. Finally, in patient 5, who was admitted for isolated traumatic head injury with acute respiratory distress associated with a refractory shock, the diagnosis of NPE was made by the medical committee on the basis of clinical manifestations respiratory distress , findings on chest radiographs, and postmortem biopsy findings.

    All subjects with neurogenic pulmonary edema had cardiac dysfunction. In this study we confirmed the presence of cardiac dysfunction in patients with NPE due to traumatic brain injury.

    Pulmonary dysfunction after acute brain injury is a common but poorly understood phenomenon. The true incidence of NPE after acute head injury is difficult to estimate because much of the information comes from small autopsy series or isolated case reports.

    Furthermore, the clinical relevance of NPE in patients with nonfatal head injury remains to be elucidated, because NPE seems to be rare in patients who survive. In Tunisia, nearly 13 persons are involved in motor vehicle crashes every year. Approximately of these patients die.

    In the study reported here, we included only patients with isolated traumatic head injury and with the typical signs and symptoms of NPE. In addition, because of a lack of tools, it was not possible to examine all patients admitted to our ICU with typical NPE. For these reasons, patients included were nonconsecutive, and we are not able to establish the incidence of this abnormality.

    NPE is characterized by an increase in extravascular lung water in patients who have sustained a sudden change in neurological condition. Increased permeability as a mechanism of NPE is supported by some studies in animals that have shown high interstitial lung lymphatic or alveolar protein concentrations 9 , 12 and time-dependent ultrastructural changes in pneumocyte type II cells after brain injury. On the other hand, hydrostatically induced pulmonary edema can occur without endothelial damage.

    One possible sequence leading to NPE is an acute increase in sympathetic tone that abruptly increases left ventricular afterload and causes intense venoconstriction, thereby elevating left ventricular filling pressures and inducing elevated pulmonary artery wedge pressures, leading to hydrostatic pulmonary edema.

    This hypothesis was confirmed by experimental studies 18 , 19 and studies in humans. In addition to these 2 hypotheses, NPE can result from a cardiac dysfunction. In fact, the early hemodynamic changes that occur in the setting of NPE may lead to the conclusion that the pulmonary edema is of cardiac origin. Smith and Matthay 9 reported, as have others, that early analysis of NPE fluid reveals a low fluid-serum protein ratio consistent with hydrostatic edema.

    In addition to the change in vascular resistance described, the pathogenesis of hydrostatic NPE may involve direct negative inotropic effects on the heart. In a retrospective study 26 that included 20 patients with NPE, all 20 required mechanical ventilation; cardiac index and left ventricular stroke work index were markedly depressed in 12 of the 20 patients; mean pulmonary artery wedge pressure was 17 mm Hg; mean pulmonary artery pressure was Patients treated with dobutamine had significant increases in cardiac index and left ventricular stroke work index and significant decreases in systemic vascular resistance index and pulmonary artery wedge pressure at 2 and 6 hours after institution of therapy and a significantly increased ratio of Pa o 2 to fraction of inspired oxygen at 6 hours after the start of therapy.

    The authors 26 concluded that NPE was generally associated with severe depression of myocardial function and elevation of pulmonary vascular pressures. This dysfunction was readily reversed by dobutamine. Neurogenic pulmonary edema may result from increased lung capillary permeability, increased pulmonary vascular hydrostatic pressure, or cardiac dysfunction.

    This hypothesis of myocardial dysfunction was supported by some echocardiographic studies. The cardiac dysfunction and wall-motion abnormalities are temporary, and cardiac function usually returns to normal.

    Our findings confirm the hypothesis of myocardial dysfunction. In addition, the control echocardiography study done in 2 patients showed a complete recovery of cardiac function. The usually reversible myocardial dysfunction shown by echocardiography is poorly correlated with ECG changes.

    Finally, our study has several limitations. Because echocardiography was not available in our ICU or in our hospital, our patients were not examined in a uniform way some were examined with echocardiography, some with pulmonary artery catheterization.

    For echocardiography to be done, the patient had to be transferred to another hospital. All patients included in our study had respiratory distress; in particular, patients 1, 3, and 7 had shock associated with acute respiratory distress with a ratio of Pa o 2 to fraction of inspired oxygen less than Therefore, we preferred to use pulmonary artery catheterization performed in our ICU in these patients.

    In patient 3, the pulmonary artery wedge pressure was normal. Despite that normal finding, the hemodynamic study of these parameters was performed after administration of a catecholamine dobutamine. The high number of patients who were excluded from the study could be a methodological limitation. Gastric aspiration and pulmonary contusion, which produce increased permeability and pulmonary edema, are potential confounding factors in clinical cases of NPE.

    We therefore believe that the elevated pulmonary artery wedge pressures could not be related to simple cardiogenic pulmonary edema.

    In addition, hemodynamic parameters determined by using pulmonary artery catheters can be difficult to interpret in patients receiving positive pressure ventilation with or without high levels of positive end-expiratory pressure.

    However, in our study, all parameters in particular, cardiac index and pulmonary artery wedge pressure were measured while the patient was receiving catecholamines, and in all patients mixed venous oxygen saturation was low, suggesting cardiac dysfunction. In this patient, who was admitted for isolated traumatic head injury with acute respiratory distress associated with a refractory shock, the diagnosis of NPE was ascertained by the medical committee on the basis of clinical manifestations respiratory distress , radiological chest radiographic findings, and results of postmortem biopsy.

    Our findings confirmed the presence of myocardial dysfunction in patients with NPE due to traumatic head injury; however, we cannot rule out other phenomena, especially permeability edema. The mechanisms of myocardial dysfunction were multiple. The great improvement in wall motion seen in 2 patients indicated the presence of a stunned but viable myocardium. User Name Password Sign In.

    Chaari , Hedi E. Previous Section Next Section. Clinical Information All 7 patients had hyperpnea and tachycardia at the time of hospital admission.

    Pulmonary edema

    Pulmonary oedema which arises due to increased pulmonary capillary pressure, in the absence of left ventricular failure, is hydrostatic. Neurogenic pulmonary edema (NPE) is characterized by acute onset of pulmonary edema after a significant injury to the central nervous. Objective: Neurogenic pulmonary edema is an underrecognized and underdiagnosed form of pulmonary com.

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