The Treatment of Acute Pulmonary Edema - Case Study Example

Running Head: Acute Pulmonary Edema Acute pulmonary Edema Name Institution Date Acute pulmonary edema is the accumulation of fluids within the alveolar spaces of the lungs that ends up with disruption of normal fluid influx within the lungs. It normally arises from the elevation of hydrostatic pressures of the pulmonary capillaries and an increase in the permeability of the alveolar capillary membranes (Kasper D, 2005). Physical findings will include: Pulmonary edema is associated with lung congestion hence most of the clinical presentations will include the features of manifestations of systemic congestion. The manifestations of congestion would range from edema of the lower limbs, congestion of the neck veins, easy fatigability and pleural effusion (Mayo clinic, 2011). Most patients will tend to be tachypneac, dyspneac, have a perspiration that is marked. Cyanosis may also be present and on auscultation bilateral rales are heard and 3rd heart sound may be heard. The patient also produces blood tinged sputum (Mayo clinic, 2010). Other symptoms will include orthopnea, tachycardia, hypertension, cold extremities, cyanosis, cough that is productive with sputum pink in color, and extensive use of accessory muscles of respiration, moist rales with or without wheezing (Mayo clinic, 2010). The patient, who is Mr. Smith presented with a productive cough that was pink tinged in color, was anxious, dyspneac, and used the accessory muscles to breath. The respiratory rate of Mr. Smith was also noted to be increased, and the saturation percentage of oxygen was at 92%.on auscultation with the stethoscope, crepitations are heard up to his scapular this shows that the fluid has greatly accumulated and has now almost reached the apices of the lungs. Causes of pulmonary edema; Pathophysiology of edema occurs in the same manner as in subcutaneous tissues. An imbalance in the starling forces is one of the causative factors of the accumulation of fluids in the interstitium and alveolus. The accumulation of fluids in the interstitium results when the mechanisms opposing the fluid transference to the interstitium which include pulmonary capillary pressure and plasma oncotic pressures. The process of fluid accumulation starts with fluid being transferred into the interstitium because of the increase in lymphatic flow increase but the net increase of interstitial volume does not occur (Kumar &Clark, 2006). What ensues will be the lymphatic’s becoming impaired in the drainage of the excess fluid and thus the fluid starts to accumulate in the interstitial spaces surrounding the bronchioles and the lung vasculature. The continued accumulation of fluid continues to build pressures in the interstitial space that is surrounding the alveoli, this leads to the impairment of gaseous exchange especially when alveoli capillary membranes becomes flooded with the fluids. Due to gravity, the fluids accumulate at the bases of the lungs and not the apices. Accumulating fluid in the lungs will only rise towards the apices only when there is a rise in the pulmonary venous pressures .The patient will then have dyspneac spells due to reduction in the amount of oxygen supply to the body, and this might be so severe that the patient might use the intercostals muscles while breathing. At this stage when the pulse oximetry is used to measure desaturation, the patient might have a low oxygen saturation levels. When the edema continues for some time, the fluid rises towards the apices and reaches the level of about 2/3rds of the lung fields, this is when the crepitations are able to be heard on auscultation (Kumar &Clark, 2006). Etiology of pulmonary edema: The causes of pulmonary edema are grouped into; The ones caused by alteration of membrane permeability which is brought by infections such as pneumonia,vaso-active substances and in some cases immunological reactions. Those resulting from Increased pulmonary capillary pressures and they involve cardiac cause such as left ventricular hypertrophy and endocarditis. On the other hand the non cardiac causes will include pulmonary venous thrombosis and congenital stenosis that originates from pulmonary veins. Other mechanisms will be due to decreased oncotic pressures which mainly results from hypoalbominaemia. Lymphatic insufficiency can also lead to edema. In this case study however, the acute pulmonary edema resulted from altered capillary permeability resulting from infection of the pulmonary edema by the pneumonic process. In the early stages of the pulmonary edema is only located within the interstitium and the patient presents with a dry cough and tachycardia, and dyspnea. The crepitations and rales start to be pronounced when the pulmonary fluid exceeds what is the normal fluid level by about three times. With the continual rapid accumulation of fluid, the patient becomes dyspneac, cyanosed and production of frothy pink sputum ensures (Kumar &Clark, 2006). Investigations: The posterior anterior and lateral chest x-ray films will show the early signs of the pulmonary edema by the visualization of Kelly b lines .As the edema progresses, the lobes of the lungs will be characterized to be having a butterfly pattern which is characterized by the central predominance of the shadows with clear zones at the peripheries. The lung will also have a butterfly like pattern. Arterial blood gases will show a marked reduction in the pao2 compared to the partial concentrations of carbon dioxide (Kumar &Clark, 2006). Management: Pulmonary edema is a medical emergency that should be managed as soon as it has been diagnosed. The patient should be place in a sitting position with the legs dangling on the side of the bed as this will make respiration easy by reducing the venous return.100% of oxygen should be delivered to the patient by a mask. Sympathetic outflow is decreased by the administration of morphine to reduce anxiety as it will cause venodilation and decrease in the preload, however it should not be given in patients with respiratory arrest.Morfine dose will be of 2 to 5mg IV bolus. Loop diuretics e.g. furosemide 40-100mg IV bolus should be given to cause venodilation and dieresis, leading to movement of the accumulated fluids from the lungs into circulation and as a result will be expelled in urine resulting in the reduction of venous return (Kumar &Clark, 2006). Nitroglycerines are also administered to reduce pulmonary edema and to also bring out venodilation. It is given when the patients’ systolic blood pressures are above 120mmhg.sublingual tablets or IV drip 0.4mg.The patient is likely to have atrial fibrillations and this will be relieved by the use of digoxin 0.25mg slow IV push as it slows the ventricular rates. Beta-adrenergic agonists or aminophyline IV are administered to relive bronchospasms that may occur in pulmonary edema and also an increase the severity of hypoxemia and dyspnea. Aminophyline will also increase renal plasmatic flow, the excretion of sodium and the increasing cardiac contractions and thus resulting in venodilation and decreased peripheral vascular resistance. Only on the instances when there is no arterial obstruction will Tourniquets be used in the limbs (3 at a time for 15 to 20 minutes) (Kumar &Clark, 2006). Role of non invasive ventilation (CPAP or BiPAP) in management of cardiogenic pulmonary edema Non Invasive Ventilation is a form of mechanical ventilation used in the provision of oxygen in critical care set up. There are two types of non invasive ventilation namely the continuous positive airway pressure and the bi-level positive airway pressure (Hillberg R et al, 1997). CPAP involves the provision of positive pressure continuously in all phases of spontaneous ventilation. It is mainly used in type 1 respiratory failure. It makes the patient take breaths at high tidal volumes hence making the lungs to become more compliant. BiPAP: involves the maintenance of Positive pressure throughout the respiratory cycle with higher pressures exhibited during or on inspiration. It is mainly used in type 2 respiratory failure (Masip J et al 2005). Mechanism of Action Non Invasive Ventilation works by improving the pulmonary mechanics and bringing about oxygenation and simply augments alveolar ventilation and goes on to allow supply of oxygen without rising of the Partial concentrations of carbon dioxide. Non Invasive Ventilation also works by resetting the respiratory centre ventilatory responses to the rising Partial concentrations of carbon dioxide (Goodacre s et al, 2008). Non Invasive Ventilation also goes on to reduce trans-diaphragmatic pressures, the pressure time index of respiratory muscles. Diaphragmatic electromyography activity is also increased and this will lead to the rise in tidal volumes, decrease of the respiratory rates and an increase in minute ventilation .Neural output to the diaphragm including the other muscles of respiration will be increased and as a result these patients will maintain a normal partial concentrations of carbon dioxide throughout the daylight hours (Bilello k, 2005). Requirements for successful non-invasive support For a successful be cooperation must be cooperative and also should be able to control their airways properly and be able to coordinate breathing properly. The secretions will be removed from the airway by coughing. The things that the nurse will be doing during the Non Invasive Ventilation process .The nurse will be taking the respiratory rates which will be the number of breaths that is delivered by the ventilator per minute with the normal’s being between 4-20 breaths per minute. The tidal volume show the volume of gases that are being delivered with every ventilator breath and will usually be of around 5-15cc/kg.Fractional inspired oxygen should also be calculated as this shows the amount of oxygen that is being delivered by the ventilator. The ratio of inspiration to expiration is also noted and here the length of inspiration is compared to that of expiration (Araújo et al, 2011). The nursing care of the mechanically ventilated Endo esophageal tube management; those who are using the endotracheal tube their care will involve, ensuring that the patient has a patent airway and the secretions from the lungs and oral cavity are removed by suction. If the patient is restless or agitated the straps holding the Endo esophageal tube management are loosened. Suction of the Endo esophageal tube management is done every two hourly and is a sterile procedure. The patients are also monitored for skin break down in the oral and nasal cavity. Oral care should also be provided eight hourly. If the patient has a bite bock to prevent them from biting the tube, it should be cleaned 8hourly.the tube should also be now and again be repositioned as this will avoid constant pressure being exerted in the same area continuously. The Endo esophageal tube management has a cuff that is normally inflated when in the trachea to hold the tube in place. The cuff should be checked 8hourly to make sure it does not exert excess pressure on the tracheal walls. After the Endo esophageal tube management care, patients respiratory status is reassessed, the insertion point of the Endo esophageal tube management in centimeters should be confirmed to being the same as the previous procedure (Plambeck A, 2011). In the tracheostomy tube, the nursing care would be; Care of the tracheostomy done every 8hourly, which involves the cleaning of the incision point. The goal of the tracheostomy care is mainly to maintain patency of the airway and also to prevent the breakdown of skin surrounding the site and to prevent infection. Patients should be observed for agitation and sedated if noted to be agitated. Sedation will make the patient to tolerate the mechanical ventilation. Sterile suction is done to the airway to remove secretions. The patient should be preoxygenated before suction to avoid hypoxemia (Plambeck A, 2011). The respiratory status of the patient is constantly reassessed and will involve the monitoring of the breath sounds four hourly and this will be both from the anterior and the posterior of the chest. Spontaneous respiratory rates and tidal volume measured as this will show the clues of the respiratory function. For example if the spontaneous tidal volume is noted to be low, it might be indicative that the patient might not do well with the weaning attempts. The measurement of the saturation of oxygen levels is done by the use of the pulse oximetry and this will this will be useful in indicating the patient’s ventilatory or acid base status. Interpretation of the arterial blood gases would also be essential in showing the ph of body fluids of the patient. The partial pressures of dissolved oxygen will be indicative of the effectiveness of ventilation (Gray A, et al, 2008). Weaning and extubation should be done at a gradual rate until the patient can be able to breathe by himself. In this period the patient’s initiative to breath starts to replace the mechanical ventilation even though it occurs progressively with time. The weaning process should only be started when the patient’s respiratory status is seen to be stable and when the patient can be aroused and can be able to follow commands given to him. The patients care in this case will involve suctioning them before the commencement of the weaning process. During the weaning process and the number of breaths supplied by the ventilator are gradually decreased (Plambeck A, 2011). Extubation involves the removal of the intubation tube after the non invasive ventilation has been completed. Prior to extubation the patient should be suctioned from both via the endotracheal tube and oral routes. The patient is made to seat up at 45 degrees during suction.Post extubation care involves the care given to the patient who has undergone intubation successfully and the intubation tube has been removed. Humidified oxygen should be delivered to the patient after extubation to prevent drying and irritation of the respiratory tract. The patient is also encouraged to undertake respiratory exercises by the nurse encouraging them to cough and also take deep breaths. This will be followed by assessment and monitoring of the patients breath sounds, the vitals being documented. In cardiac pulmonary oxygenation hence increase edema, Non Invasive Ventilation has shown to improve the cardiac output and at the same time reducing the work of breathing.niv has shown to be effective in the patients who have hypercapnea (Plambeck A, 2011). Benefits of non invasive ventilation in the management of pulmonary edema The patient using the Non Invasive Ventilation will benefit since the airways mechanism of defense will usually preserved when this method is used to provide oxygen. Non Invasive Ventilation goes in the long run to offer timely early and timely ventilator support to the patient. Use of Non Invasive Ventilation offers intermittent ventilation hence this will help especially when the patient is undergoing spells of dyspnea. The use of the Non Invasive Ventilation also enables the patient to feed, drink and communicate normally (Sandham J, 2011). Application of Non Invasive Ventilation is done with ease with also the Non Invasive Ventilation removal not being cumbersome compared to the other method the patients comfort. However less sedation is required while using the Non Invasive Ventilation with intubation being avoided since it is associated with complicates. The Non Invasive Ventilation also generally improves the patients comfort (Sandham J, 2011). Conclusion: Management of pulmonary edema is started once the diagnosis has been confirmed since it’s a medical emergency. Use of non invasive ventilation has shown success in the management of the pulmonary edema. Provision of care to a patient with pulmonary edema will require adequate care to be given right from the time of intubation up to the post extubation period. References Plambeck A, 2011 adult ventilation management, 7.9 nursing contacting hours, accessed on 8th April, 2011 from http://www.corexcel.com/courses/Vent_Web_Handout. Gray A, et al, 2008. Non invasive ventilation in acute cardiogenic pulmonary edema, The England Journal of Medicine. Sandham J, 2011 the need for mechanical ventilation, Non-invasive ventilation http://www.ebme.co.uk/arts/ni_vent/ Mayo clinic, 2010 Pulmonary edema, symptoms http://www.mayoclinic.com/health/pulmonary- edema/DS00412/DSECTION=symptoms Masip J et al 2005 Noninvasive Ventilation in acute Cardiogenic Pulmonary Edema, American Medical Association. jama.ama-assn.org Goodacre s et al, 2008 the participants in the Three Interventions in Cardiogenic, Pulmonaryedema,CardiogenicPulmonary http://www.nejm.org/doi/pdf/10.1056/NEJMoa0707992 Bilello k, 2005. Non invasive ventilation for acute respiratory failure. http://www-archive.thoracic.org/sections/chapters/thoracic-society-chapters/ca/current- news/resources/KBNoninvasiveVentForAcuteRespFailure.pdf Araújo et al, 2011 acute pulmonary edema, Intensive Care http://www.medstudents.com.br/terin/terin7.htm Hillberg R et al, 1997 noninvasive ventilation, Massachusetts medical Society. Kasper D, 2005.acute pulmonary edema, Harrison’s Principles of internal Medicine, McGraw Hill 13th edition. Kumar & Clark, 2006 acute pulmonary edema, clinical medicine, 7th edition. Elsevier Inc. . Read More