Pulmonary edema caused by left sided heart failure,ed sheeran london ontario june 5 2015 review,list of communication skills in health and social care - PDF Books

Patients with pulmonary edema may undergo phlebotomy procedures to decrease their total blood volume. The two main types of Pulmonary Oedema this essay will aim to evaluate are known as Interstitial and Alveolar Oedema. Pulmonary Oedema, usually resulting from left sided heart failure, is fluid accumulation in the lungs which can happen due to inadequate functioning of the heart or circulatory system.
The second is known as Interstitial Oedema which occurs initially when a build up of pressure pushes the fluid out of the alveoli and into the surrounding tissue.
Heart failure is recognized as being the most common cause of the illness and the number of patients, mainly elderly, seems to be increasing. This evidence suggests that Pulmonary Oedema is becoming more prevalent in the UK, also compelling healthcare professionals to recognize it as an illness generally associated with the elderly. However, there are other causes of Pulmonary Oedema that would lead one to believe that it should not necessarily be an illness solely associated with the elderly. There are many different symptoms of Pulmonary Oedema, and some may be easier to recognise than others. The main symptom of Pulmonary Oedema can be recognized if the patient is experiencing difficulty in breathing.
The classic signs of Pulmonary Oedema can be the production of pink frothy phlegm, swelling of certain limbs such as the ankles or hands, anxiety, wheezing and restlessness. In conclusion, this essay has hopefully gathered a sufficient amount of evidence to suggest the condition is becoming more prevalent in the UK, and that increasing numbers of patients with the illness are predominantly associated with the elderly. Inasmuch, it can also occur as a result of inflicted social behaviour which can be implemented from any age group. 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. This particular field of study has been chosen and this essay will aim to analyse and evaluate the condition, as well as briefly identifying which kind of patient the illness is generally associated with .
Heart failure is recognised as one of the most common causes of the illness and this essay will also aim to gather and analyse evidence to support this claim. It can be a result of cardiac disorders and can appear as a chronic condition or develop quickly, rapidly becoming fatal (Springhouse 2003).
The first, known as Alveolar Oedema, is a condition in which the alveoli of the lung become filled with fluid, and can therefore appear opaque to x-rays. This can be caused by Multi trauma, illicit drug use particularly cocaine, and from a Haemorrhage to the subarachnoid space of the brain. This claim is supported by McDonagh et al (1997) cited by Coady (2002:41) who claimed that heart failure is predominantly a disease of the elderly and in the UK, prevalence of symptomatic heart failure increases with age to about 10 percent in those aged over seventy five years and it continues to rise.

Such causes could be pneumonia, head injury, mercury poisoning or even near drowning as these causes can occur in people of any age. In the case of Alveolar Oedema the patient may be showing external signs of Pulmonary Oedema, but due to the condition being opaque to x-rays medical professionals may find it difficult to diagnose from evidence based on internal symptoms especially if the condition is in its early stages and no infections or noticeable lung damage has been induced. Depending on the stage of development of the condition; breathing difficulties may vary in accordance with severity. Atozdiseases (2007) claim that in a severe attack patients may also turn bluish as there is an insufficient amount of oxygen in the blood. The information presented shows that Pulmonary Oedema can generally be a condition associated with elderly patients, usually induced from inadequate cardiac or respiratory function. This essay has hopefully given a clear insight into the symptomatic changes the body can go through, as well as looking at the main causes of Alveolar and Interstitial Pulmonary Oedema. 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 claim is also supported the statement that if it is left untreated it can lead to coma or even death.
In this circumstance, treatment can be delayed if the external symptoms are not recognized and it is the fluid inside the alveoli septa that usually fills the airspace. If this is present for a long time the patient may become more susceptible to infection as well as sustaining acute injury to the lung.
If the patient is repositioned upright breathing can become more manageable, it does not resolve the condition completely but can help manage comfort levels if only temporarily. It is the same fluid accumulation that can prevent oxygen from filling the alveoli, and in turn can also stop the oxygen from being absorbed into the bloodstream. Some of the common causes for this condition are usually inhalation of toxic gases, severe infection, aspiration or even multiple blood transfusions.

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