Non-Invasive Ventilation - Case Study Example

 Non-invasive ventilation The case Mr Smith was a 38 year old male who had been transferred to the acute medical ward from the Emergency Department. He had a past history of acute myocardial infarction six months ago. He had presented with a one week history of chest cough, fever, shakes and five days of expectorating tenacious yellow green sputum, decreased appetite and mild right sided chest pain with increasing dyspnoea. Repeated tests confirmed that he had right sided middle lobe pneumonia. Mr Smith had pathology and radiology investigations ordered in the ED. His results were as follows: Symbol Full form Result Normal range Na+ Sodium 132mmol/L 135-145 mmol/L BGL Blood glucose level 8.5mmol/L 3.5-7.8 mmol/L K+ Potassium 3.2mmol/L 3.5-5.0 mmol/L Cr Creatinine 99 µmol/L 50-90 µmol/L CRP C-reactive protein 287mg/L 1-3 mg/L eGRF Glomerular filtration rate >90 (95-145mL/min/1.73m²) Hb Haemoglobin 130g/L. 140-174 g/L WCC White cell count 12.89x 109/L 4-10 X 109/L Table 1 Investigation results of Mr. Smith Chest X-ray showed right middle lobe pneumonia. Being a non-smoker, Mr.Smith had not travelled overseas and had no exotic pets. Clinical assessment Mr Smith had scored 15 on the Glasgow Coma Score (Trauma-org). This indicated that Mr. Smith was having the best score and that he was in a good clinical condition where his neuropsychological status was concerned. This meant that he had his eyes open and they were responding. He was oriented, answering questions and obeying commands. Mildly febrile, he had accompanying tachycardia and his pulse had changed from the normal 72 beats per minute to 98 per minute. This could be partly due to the raised temperature and partly due to the progression to acute pulmonary oedema. The middle lobe had an anatomy which predisposes it to frequent involvement. The narrowness of the lobar bronchus and the acute angle at which it took off made it prone to difficulties of drainage. Pneumonia formed one cause of non-obstructive middle lobe syndrome (Bordow et al, 2005). The isolated position of the middle lobe also produced an impairment of collateral ventilation from the neighbouring lobes. Clearance of secretions was simultaneously defective. Inflammations constituted 47% of middle lobe syndrome in researches (Bordow et al, 2005). The history of symptoms of cough, fever with chills and the expectoration that Mr.Smith presented with correlated to the middle lobe pneumonia. Frontal and lateral chest X-rays provided the best pictures of the middle lobe. The Blood Glucose level was a little raised from the normal. He could be a borderline diabetic who needed to be watched and advised for a sugar-free diet. The stress due to the illness also could raise the glucose level. Investigation at intervals could help in the diagnosis. The electrolyte levels were slightly less than normal. Due to the fever and illness of the past five days, he could have reduced his food intake. Potassium reduction could also have been due to dehydration through excessive sweating following the fever. Serum creatinine was just above normal level. The glomerular filtration rate was however near normal. Repetition of the investigations would help in deciding whether the patient was going in for other complications. Haemoglobin level was slightly less suggesting again that dietary intake could have been less. Caution must be taken to prevent anaemia. The high CRP level at 287 mg/L was indicative of the previous history of MI in Mr.Smith. It could also be an accompaniment of the middle lobe pneumonia, an infectious process. BP was slightly raised. Respiratory rate was 20/min. with shallow breathing. The saturated oxygen level was 98% using a 6-litre Hudson mask and it was the percentage of hemoglobin saturated with oxygen at the time of the measurement. The 98% was a favorable level but the best was the 100% saturation. An indwelling catheter had been inserted. An IV access was also found. Subsequent assessment In the assessment after one hour, the condition of the patient had changed to a more critical one. Patient had become anxious and was breathing heavily and using his accessory muscles to do so. Respiratory rate had increased and he started coughing up pink-colored sputum. On auscultation, fine and coarse crepitations could be heard up to the scapula. The MET made a diagnosis of acute pulmonary edema. The management was to use non-invasive ventilation and intravenous dosage of 2.5 mg. morphine and 40 mg.of frusemide. Diagnosis Mar. Smith was diagnosed with acute pulmonary enema following middle lobar pneumonia, a non-cardiac cause, with the clinical features of tachypnoea, tachycardia, dyspnoea at rest, severe hypoxemia and pink coloured sputum. Mr.Smith was also anxious about his condition. The investigations and chest X-ray confirmed the diagnosis (Localzo, 2010). ECG was not done for him. Pathophysiology of pulmonary oedema To understand what happened to Mr.Smith’s respiratory system and why it went into a compromised situation, the normal physiology must be understood. In the normal respiratory system, air entered the lungs during inspiration and exited during expiration. It then passed through the airways of the respiratory tract from the trachea to the alveoli through the bronchi. The capillaries of the lungs adjoining the alveoli brought deoxygenated blood from the different parts of the body to undergo oxygenation at this level. Gas exchange occurred in the alveoli and oxygenated blood was carried away to be distributed by the heart to the various parts of the body. At the cellular level, the “hydrostatic pressure of the capillaries, the oncotic pressure, capillary permeability and the lymphatic drainage” had an existing balance among them (Professional guide, 2010). The upset of this balance caused the flow of fluid into the alveoli. When the left ventricle failed, its filling pressures were increased. The capillary hydrostatic pressure was then elevated to compensate so that cardiac output remained the same. The pressures then got transferred to the atrium, pulmonary veins and capillaries. The steady rise in the capillary hydrostatic pressure forced passage of solutes and fluids from the capillary bed into the interstitial tissue. The alveoli got flooded, first interrupting the gas exchange. Pulmonary oedema was the result (Professional guide, 2010). The passage of fluids into the larger airways produced the lung stiffness and impaired expansion (Porth and Matfin, 2010). Poor oxygenation occurred due to the collection of fluids in the alveoli. Inspiration and expiration were normally possible by the contraction and relaxation of the diaphragm respectively. The accessory muscles of respiration were the sternocleidomastoid, scalene, pectoralis major, trapezius, internal intercostal, and abdominal muscles. They came into action only when the diaphragm and external intercostal were unable to increase their action to counter the defective oxygenation (Porth and Matfin, 2010). Mr.Smith had dyspnoea which was the clinical feature seen when the oxygenation process in the lungs was defective and the action of the diaphragm and external intercostal became enhanced. The inspiration and the expiration could not bring about the same amount of gas exchange in the alveoli to enable the oxygenation. Then the body attempted to enhance oxygenation by putting the accessory muscles of respiration into action hoping to correct the situation. The oxygen saturation as indicated by the pulse oximeter was reduced when oxygenation started to fail. When fluids began to fill the alveoli and the airways, tachypnoea was seen. Cyanosis was then evident in the nail beds and lips due to defective oxygenation. Severe pulmonary oedema was characterised by the gasping patient in an effort to increase oxygenation (Porth and Matfin, 2010). A rapid pulse, moist skin and cyanotic features were diagnostic of severe pulmonary oedema. The further decrease in oxygenated blood supply affected the brain and the patient could be stuporous and then go into coma. Mr Smith was having a score of 15 on the Glasgow Coma Scale in the beginning. He was quite normal in demeanour then. However later his anxiety increased due to the changes in the brain caused by the highly deoxygenated state of the circulating blood (Porth and Matfin, 2010). The productive cough with pink frothy sputum was caused by the mixing of air with serum albumin and RBCs which had passed into the alveoli. The frothy effect was due to the serum albumin in the fluids. The fine crepitations or crackling on auscultation were the earliest indication of fluids in the alveoli. The passage of fluids into the larger airways produced the coarse crepitations. The sound was produced by the air moving through the fluids. Nursing Interventions .Core interventions for nursing in non-invasive ventilation. 1. Airway management 2. Oxygen therapy 3. Therapeutic management 4. Ongoing assessment and monitoring of vital signs 5. Oral care Airway management The airway was maintained to make sure about the oxygenation and the maintenance of perfusion (Kovacs and Law, 2007). Airway management was of utmost significance in an emergency. The securing of an airway usually followed a respiratory assessment. Airway block could be caused by vomit, secretions, artificial dentures, foreign bodies and even fractured pieces of the mandible or laryngeal bones (Higginson et al, 2010). If the airway was closed, the head could be tilted and the chin lifted to open it. Using the fingers under the chin, the mandible could be lifted upward and outward. Neck injury was excluded before doing this procedure. Mr. Smith’s airway could be easily managed as there was no history of injury or fracture neck region. His airway was not in a compromised situation. Suction clearance was an inevitable part of keeping the airway open and intact during ventilation. Secretions were usually coughed out by the patients themselves. In the possibility of the patient being unable to cough, the nurse had to clear the secretions manually or otherwise (Higginson et al, 2010). In non-invasive oxygen therapy, a Yankauer sucker could be used. If endotracheal intubation had been done, this tube had to be sucked. The airway maintenance, oxygen supplementation and gaseous exchange could be improved with the suction. The correct size of suction catheter could be calculated by the formula below. suction catheter size = ET tube size x 3 2 Oxygen therapy The haemoglobin saturation could affect the color of the skin. Observation of the color of the skin was a rapid indicator of the saturation level. The determination of the oxygen saturation by using the non-invasive method of pulse oximetry had limitations. The hypoventilation in a patient who was receiving continuous supplemental oxygen could not be detected (Higginson et al, 2010). ABG analysis or arterial blood gas analysis was the other method of assessing oxygenation; the partial pressures of oxygen and carbon di-oxide provided the information (White et al, 2010). This could prevent metabolic impairments (hyperventilation could produce acidosis). The quantity of carbon dioxide in the blood would be indicated by the Partial pressure. The end-tidal carbon dioxide monitor determined the amount expelled from the lungs. The normal value was 40 mm Hg or 5%. Mr.Smith could have a larger value as he had respiratory illness (Oh et al, 2003). The value of the oxygen saturation was not as indicative of the patient’s condition as the change that occurred in the patient. Whether he was improving with the supplemental oxygen or worsening was more important for assessment. Maintaining the saturation level as close to normal as possible was essential. The probe of the pulse oximeter should be in an ideal position to get the best results. False results could be obtained if the placing was improper or if the patient had low blood pressure or if he were cold and sweaty. Patients with chronic obstructive pulmonary disease or emphysema could have false results too. Mr Smith had an arterial oxygen saturation of 98% as recorded by the pulse oximeter in the first clinical assessment (Schutz, 2001). Due to the impairment in the oxygenation process, the oxygen in the blood was diminishing. The figure was 92% in the subsequent assessment. This indicated the worsening of the critical condition of Mr.Smith. Tachypnoea and the acting accessory muscles attempted to improve the oxygenation. Cyanosis exhibited by the bluish nail beds and lips also was another result. Knowing when exactly to administer oxygen was essential. The safe delivery of sufficient oxygen based on the patient’s need was the responsibility of the nurse (Higginson et al, 2010). Two delivery systems were recognised: the variable performance and the fixed performance. Using the variable performance systems, the exact measurement of oxygen delivered could not be understood. The Hudson mask, non-breathing mask with a reservoir and the nasal cannula were the variable performance systems. With the fixed performance systems, the exact amount of oxygen could be delivered. The “high airflow enrichment mask” or the “Venturi mask” was a fixed performance system. The administration of supplementary oxygen depended on the breathing ability of the patient. When voluntary breathing stopped, endotracheal intubation had to be done as an emergency procedure (Higginson et al, 2010). The size of the tube could vary with the size of the patient. When an airway was compromised and could remain so for a long duration, tracheostomy, a surgical procedure, needed to be done (Veelo et al, 2008). The tracheostomy also allowed easy removal of secretions (Trouillet et al, 2010). Tracheostomy tubes were placed with cuffs inflated to 15-22mmHg into the trachea directly by making an opening surgically (Higginson et al, 2010). The pressure in the cuff was to be checked often and the cuff was frequently deflated and again inflated to release the pressure on the surrounding tissues at intervals. Suction was done with the cuff inflated and above it to remove the secretions. Tracheostomy had complications like chest infection. Close monitoring was essential whichever method had been adopted.(Higginson et al, 2010). Therapeutic management Treatment Plan 1. Supplemental oxygen to improve oxygen saturation which had been compromised 2. Morphine injection Dose 3.5 mg as an IV solution of 1mg/ml. and given at the rate of 1mg/minute. 3. Diuretic 40-80mg IV to be repeated if necessary. 4. Non-invasive ventilation to help the compromised respiratory functions. 5. Continuing care at home. The goal of treatment was to ensure that Mr. Smith recovered from his pulmonary edema and his respiratory system came back to normal. He must be taken off the non-invasive ventilation and allowed to go home with a maintenance management plan. The plan could be put into action with the collaboration of the family and the friends of Mr.Smith after the acute stage of illness was covered and the patient was on the road to recovery. The anxiety that Mr.Smith had experienced could be reduced by the kind words of the physician, the nurses and the family. In the psychobiological model, the patient who was worried about his complaints and illness, approached the physician who convinced the patient that he knew all about the illness and was willing to treat him. If he was not better, he would get him treated by another specialist friend of his. This created a feeling of confidence in the patient. Such a model was evident in this situation. Mr. Smith was waiting to go back home after treatment. The medicines to be administered to the patient had to be provided at the correct time and in the correct dosage as prescribed by the physicians (White et al, 2010). The functions of the medicines needed to be understood and side-effects were to be watched for. Mr. Smith had been prescribed morphine, an opiate. The vasodilatation and the venous pooling in the periphery were the actions of Morphine which helped to decrease pulmonary congestion. The anxiolytic action of morphine was useful to Mr.Smith (Sosnowski, 2008). However the use of opiates was being questioned in recent times. Some researchers had even attributed a worsening of the acute pulmonary edema to the use of opiates (Flutowski et al, 2003). Some researchers believed that morphine could not be administered in the initial stages of acute pulmonary edema. Morphine was a vasodilator which had a histamine-like effect and was transient in action. It was administered as a solution of morphine sulphate diluted as1mg/ml as an IV administration at a rate of 1mg/minute and the dose given was 3-5 mg. (Khan, 2007). The dose could be administered again after 15 or 30 minutes and repeated til a beneficial effect was seen. The total dose possible was 10-15 mg. The diuretic Frusemide was given at a dose of 40-80 mg IV injection which could be repeated if necessary after 30 minutes if the blood pressure was stable. Its venodilator action usually provided relief within ten minutes (Khan, 2007). Severe hypotension could be a side-effect and had to be looked out for. Ongoing assessment and monitoring of vital signs. The efficiency of the respiratory system needed to be assessed repeatedly by determining the rate and auscultated breath sounds (White et al, 2010). Management could be as ordered by the physician... Respiratory problems could be expected if the patient was found to purse his lips as if going to whistle or show flared nostrils. Speaking in monosyllables was another indicator (Higginson et al, 2010). Real distress also called the accessory muscles into action. The breathing rate, rhythm and depth of respiration were to be watched. Chest wall expansion needed to be bilaterally equal on both sides and effective in both inspiration and expiration (Higginson et al, 2010). Paradoxical movements should not occur. These included the movement of only one side, movement more on one side or the two sides moving in opposite directions. Vital signs like the temperature, nature of pulse, heart rate at the apex, blood pressure and oxygen saturation needed to be assessed on an ongoing basis. Frequent assessment of the blood pressure and heart rate at the apex were significant in the monitoring of the cardiovascular system (White et al, 2010). Pulse oximetry assessments were to be frequently made to maintain the oxygen saturation at 95% or more as the physician ordered. Supplemental oxygen was to be given if the saturation decreased. The decrease should never occur due to infrequent assessment. Electrolyte values were to be monitored (White et al, 2010). Oral care Oral hygiene needed to have a priority in the management of ventilated patients (Lizy et al, 2009). Sponge toothettes could be used for maintaining oral hygiene. Research had revealed that nurses considered oral care as high in their priority. However 68% of nurses in a study found it difficult to clean the patient’s mouth and 40% found it unpleasant. 73% requested for more equipment and better supplies (Lizy et al, 2009). The oral hygiene could reduce the incidence of pneumonia which ventilated patients had a tendency to develop. Benefit of non-invasive ventilation in the acute management of APO. Mr. Smith had non-invasive ventilation instituted so as to bring him out of the acute pulmonary edema and the associated respiratory compromise. Non-invasive ventilation produced augmentation of the alveolar ventilation by enabling both the inspiratory (IPAP) and expiratory (EPAP) positive airway pressure (Ganfyd, 2007). Gas exchange within the alveoli was improved by the tidal volume and minute volume and IPAP was responsible for the better tidal volume (McBrien, 2009). Alveolar ventilation was promoted by the EPAP. This also helped to increase gas exchange and prevent the collapse of the alveoli. Increased IPAP further facilitated the removal of carbon dioxide. The EPAP enhanced the oxygenation of the patient in ventilation (Ganfyd, 2007). The NIV assisted in changing the respiratory compromise in acute pulmonary oedema through various mechanisms. The spontaneous respiratory effort was increased by the NIV. Gas exchange was enhanced. The intrapulmonary shunt was reduced. The respiratory muscles were allowed to rest. Dyspnoea was relieved by the non-invasive ventilation (Lightowler et al, 2003). Non-invasive ventilation needed to be done in the midst of trained staff. Non-invasive ventilation relieved the respiratory compromise of acute pulmonary edema as in Mr.Smith. It also diminished the requirement for oxygen therapy as the patient recovered and took over his own respiration. Fatal complications were reduced. The incidence of endotracheal intubation and hospital stay were also decreased (McBrien, 2009). However for a person with a compromised airway, either a Guedel airway or intubation of the trachea could be done. If the airway was severely compromised, cricothyroidotomy or emergency tracheostomy could help (Higginson et al, 2010). My experiences as a nurse This case study had helped me find my strengths and weaknesses. My knowledge constitutes just the tip of the iceberg. One single topic has taught me new evidence-based practices regarding acute pulmonary edema and non-invasive ventilation and its benefits for the acute pulmonary edema. The vast expanse of research is just waiting for me to explore further and contribute to it. Saving a patient through dedicated work and sincerity is the theme of my profession. Incorporating my whole attention to my chosen job would enrich my knowledge and experience and change me into a competent senior nurse leader. Nursing ethics binds me to produce the best I have for the profession. Attending to a patient in acute care is as much a responsibility as it is a legally binding necessity. References: Accessory muscle use, http://www.wrongdiagnosis.com/symptoms/muscle_symptoms/book-causes-14b.htm Health Grades Inc. Bordow, R.A., Ries, A.L. and Morris, T.A. (2005). Manual of Clinical Problems in pulmonary medicine. Lippincott,Williams and Wilkins Fiutowski M, Waszyrowski T, Krzeminska-Pakula M, Kasprzak JD. (2003) Wpływ leczenia farmakologicznego na rokowanie krótkoterminowei długoterminowe u pacjentów po incydencie kardiogennegoobrze˛ku, płuc (Relationship of medical therapy and survival in patients after acute cardiogenic pulmonary oedema). Polski Przeglad Kardiologiczny 2003; 5: 409–14. Frankel, R.M., Quill, T.E. and McDaniel, S.H. (2003). The biopsychosocial approach: Pat present and future Rochester Press. Ganfyd (2007) Non-Invasive Ventilation. www.ganfyd.org/index.php?title=Non-invasive_ ventilation (Last accessed: April 9th , 2011.) Glasgow Coma Score http://www.trauma.org/archive/scores/gcs.html. Trauma-org. Higginson, R., Jones, B. and Davies, K. (2010). Airway management for nurses: emergency assessment and care. British Journal of Nursing, 2010, Vol 19, No 16 Mark Allen Publishing Ltd. Khan, M.I.G. (2007) Cardiac drug therapy. Humana Press. Kovacs, G. and Law, J.A. (2007). Airway management in emergencies. McGraw Profesional Leach, R.M. , Ward, J.P.T. and Sylvester, J.T. (2004). Critical care medicine at a glance Wiley-Blackwell. Lightowler, JV, Wedzicha, JA, Elliot, MW et al (2003) Non-invasive positive pressure ventilation to treat respiratory failure resulting from exacerbations of chronic obstructive pulmonary disease: Cochrane systematic review and meta-analysis. British Medical Journal. 326, 177-178. 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