Acute Pulmonary Oedema - Essay Example

Running Head: ACUTE PULMONARY OEDEMA Acute Pulmonary Oedema Name Institution Acute Pulmonary Oedema Introduction Acute pulmonary oedema is the name that is used to refer to the extravasation of the fluid that comes from the pulmonary vasculature and fills the alveoli and the interstitium of the lung. This occurs when the left atrium venous and pulmonary veins return is more than that of the left ventricular (LV) output. Pulmonary oedema may be as a result of the following pathophysiologic mechanisms; lymphatic obstruction, the disparity of Starling forces (which refers to an increase in capillary pressure, a reduction in plasma oncotic pressure, a rise in the negative interstitial pressure), lymphatic obstruction, impairment of the alveolar capillary barrier and idiopathic mechanisms such as elevated hydrostatic pressure (Australian Emergency Nursing Journal, 1999). Elevated hydrostatic pressure that results into pulmonary oedema may be caused by; an increased intravascular volume organization, the obstruction of pulmonary venous outflow or the failure of the left ventricle which is subsidiary to the diastolic or systolic dysfunction associated with the left ventricle. Pulmonary oedema results in the rapid wear and tear of the alveolar gas exchange and thus respiratory failure. Ambulance management and nursing management are usually done before the patient is attended by a doctor. Ambulance management involves resuscitation when necessary, sitting up of the patient and the administration of relaxers. Nursing management that takes place in the Emergency Department (ED) is geared towards the relief of hypoxia, the reduction of myocardial oxygen demand (MVO2) and the reduction of fluid overload. Therapy at hand is immensely supportive of the nursing management. It is noted that heart failure which is linked to Acute Pulmonary Oedema is a sensitive medical emergency that requires prompt intervention (Australian Emergency Nursing Journal, 1). Pathophysiology Pulmonary oedema is caused due to increased pulmonary capillary hydrostatic pressure that leads to the transudation of fluid that goes into the alveoli and the pulmonary interstitium. Pulmonary venous pressure is increased by the left atrial pressure and consequently an increase in the lung microvasculature pressure which results into pulmonary oedema. Mechanism The separation between the pulmonary capillary blood and the alveolar gas is done via the alveolar-capillary membrane which constitutes 3 anatomically different layers; alveolar epithelium, capillary endothelium and interstitial space which may be constituent of connective tissue, macrophages, fibroblasts and connective tissue. Pulmonary oedema is thought to take place as a result of an increase in the fluid net flux that comes from the vasculature and moves into the interstitial space. The fluid balance is determined by the Starling relationship that exists between the vascular bed and the alveoli (Australian Emergency Nursing Journal, 1). The following is an equation that determines fluid net flow: Q = K (P cap -P is) - l(Pcap - Pis), Q net fluid filtration; K filtration coefficient; P cap capillary hydrostatic pressure, that forces fluid out of the capillary; P is interstitial hydrostatic pressure, that forces fluid into capillary; l reflection coefficient, that indicates effectiveness of capillary wall thus prevents protein filtration; Pcap plasma colloid osmotic pressure, that pulls fluid into capillary; and Pis interstitial fluid colloid osmotic pressure, that draws fluid out of capillary. The fluid net filtration may be increased as a result of the changes that take place in the different parameters that constitute that Starling equation. Pulmonary oedema greatly takes place subsidiary to an increase in the pressure of the pulmonary capillary. It also takes place subsidiary to the impairment of the left atrial outflow or as a result of the Left Ventricle dysfunction. For the secondary development of pulmonary oedema to an elevated pulmonary capillary pressure, it is required for the pulmonary capillary pressure to rise higher as considered to the osmotic pressure of the plasma colloid. In normal conditions the colloid pressure is 28 mm Hg and the pulmonary pressure is 8-12 mm Hg. The pressure of the high pulmonary capillary wedge (PCWP) may not be obvious in established pulmonary oedema due to the normalization of the conditions during the measurement of the pressures (Australian Nursing Journal, 1). Lymphatics Lymphatics play a vital role in the maintenance of appropriate fluid balance that exists in the lungs through the removal of colloid, solutes and liquid that comes from interstitial space at 10-20 mL/h. Fluid filtration that takes place into the lung interstitium may result into a spike in the pulmonary arterial capillary pressure to more than 18 mm Hg, on the other hand; there is not a corresponding increase in the removal of the lymphatic. It has been noted that in situations where there exists elevated pressure of the left atrial, the rate at which the lymphatic is removed can be approximately 200 mL/h, this rate shields the lungs against pulmonary edema. Stages Pulmonary oedema takes place in a series of 3 physiologic steps; the first stage is depicted with an elevated pressure of the left atrial. This results in the distention and thus the opening of minute pulmonary vessels. There is no deterioration of blood gas exchange and can thus be improved. The second stage is depicted by the movement of colloid and fluid from the capillaries into the lung interstitium. It is however noted that a rise in the lymphatic outflow serves to remove the fluid. The continuous filtration of the solutes and liquids may overwhelm the capacity of drainage that can be conducted by the lymphatics. In this situation, the fluid first accumulates in the comparatively compliant interstitial compartment (Australian Nursing Journal, 1). This compartment is usually the perivascular tissue that forms part of the large vessels that is situated in the dependent areas. The collection of fluid that takes place inside the interstitium may serve to compromise the minute airways which results into mild hypoxemia. The hypoxemia that manifests itself at this level is more often than not of insufficient size to stimulate tachypnea. Tachypnea is largely as a result of the stimulation of the capillary; juxtapulmonary with (J-type) receptors. The receptors are nonmyelinated nerve endings which are located next to the alveoli. J-type receptors take part in the modulation of heart rates and respiration. In the third stage; fluid collects in the interstitial space which takes place due to an increase in fluid filtration which results in the filling of the free interstitial space. Fluid can fill the interstitial space up to 500 mL. As a result of the accumulation of fluid more and more fluid in the alveoli; flooding of the alveolar may take place. At this level; there must be noticeable abnormalities in the gas exchange, there is severe hypoxemia, there is a reduction in respiratory volumes and vital capacity. Pathophysiologic considerations Pulmonary oedema usually takes place as subsidiary to the impairment of the left atrial or due to the dysfunction of the left ventricle. The left atrial outflow reparation may be chronic or acute. Chronic impairment may be due to left atrial tumors and mitral stenosis. There might be an increase in the heart rate which may take place subsidiary to atrial fibrillation which eventually results into pulmonary oedema which emanates from a reduction in the Left Ventricular filling. An increase in the left ventricle pressure is achieved due to acute mitral valve regurgitation subsidiary to the dysfunction of the papillary muscle or the rupture of chordae tendineae and thus results into pulmonary edema (Australian Emergency Nursing Journal, 1). The dysfunction of the left ventricle may either by diastolic or systolic or due to both actions. It may also be linked to the overload of the left ventricle volume or the obstruction of the outflow of the left ventricle. Systolic dysfunction which is a cause of pulmonary oedema is described as a reduction in myocardial contractility that results into cardiac output. Sympathetic activity is stimulated by a drop in cardiac output and an expansion of the volume of the blood by the activation of renin-angiotensin-aldosterone system, which results into reparation by a decrease in the time it takes to fill the left ventricle and thus an increase in the capillary hydrostatic pressure. A decrease in the diastolic distensibility (compliance) is signaled by a diastolic dysfunction. This results into a heightened diastolic pressure requirement so as to obtain a similar stroke volume. Hydrostatic pulmonary oedema is generated despite of the normal contractility of the left ventricle and hence a reduction in the cardiac output that takes place in association to excessive end-diastolic pressure. Abnormalities of diastolic nature may be as a result of constriction and restriction. The overload of the left ventricle volume may be as a result of non-cardiac or cardiac conditions. Cardiac conditions are those which are as a result of chronic mitral regurgitation, the rupture of the ventricular septal, chronic or aortic insufficiency. Noncardiac condition is that of volume overload. The aforementioned conditions result in an elevation of the left ventricle’s end diastolic pressure and the pressure of the left atrial which results into pulmonary oedema. An obstruction of the left ventricle which may be caused by aortic stenosis results to an increase in the pressure of filling the end-diastolic and also an increase in the pressure of the pulmonary capillary. The rise in the pressure of the right aterial pressure and the left atrial pressure gives rise to the peripheral oedema and pulmonary oedema respectively which is caused by cardiac tamponade (Australian Emergency Nursing Journal, 1). Self-perpetuating cycle of events take place in the cardiopulmonary system in the wake of the onset of pulmonary oedema. The cycle is began in the event of the systolic dysfunction of the left ventricle which reduces cardiac output and myocardial contractility thus resulting into the activation of the renin-angiotensin-aldosterone system and the stimulation of catecholamine production. Due to the aforementioned events; there is an increase in the resistance of systemic vascular which leads to an increased wall tension myocardial, the ischemia of the myocardial, and the deterioration of cardiac output and LV function, all these events perpetuate the cycle. Myocardial wall tension increase leads to synchronized diastolic dysfunction, which leads to an increase of pulmonary capillary and pulmonary artery pressures. There is an occurrence of transudation of in the alveoli and pulmonary interstitium in the event the capillary hydrostatic pressure is more than the pulmonary interstitial pressure. Description Victorian (aust) Emergency Ambulance Management of Acute Pulmonary Oedema Nursing management that takes place in the Emergency Department (ED) is geared towards the relief of hypoxia, the reduction of myocardial oxygen demand (MVO2) and the reduction of fluid overload. It entails; oxygen administration accompanied with blood gases monitoring to make sure that hypercapnia is avoided; insertion of cannula IV is required. The following actions are taken in the ambulance; resuscitation is done when necessary, the patient is sat up, oxygen is administered to the patient via face mask that is if available, a IV cannula is inserted into the patient and analgesia, nitrates and furosemide administered. The patient is then rushed to hospital for further procedures. References: 1. Australian Emergency Nursing Journal (1999). Left Ventricular Systolic Heart Failure Resulting in Acute Pulmonary Oedema; Pathophysiology and Nursing Management in the Emergency Department. Volume 2. 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