Respiratory failure - Case Study Example

Case Study-Based Assignment Question On general physical examination, Wilson had increased respiratory rate (28 breaths per minute), deep and laboured breathing and saturations of 89 percent on oxygen of 6L per minute. Respiratory system examination revealed intercostal muscle recession on inspection and diminished air entry to both bases and crepitations in the right base on auscultation. Arterial blood gas analysis revealed PaO2 less than 60mmHg (58mmHg) and PaCO2 more than 50 mmHg (54mmHg) with pH of 7.3. These are the four pieces of evidence pointing towards acute respiratory failure. Respiratory failure is a condition in which the function of the respiratory system has altered in such a way that the partial pressure of oxygen or PaO2 is less than 50mmHg with or without rise in the partial pressure of carbon-di-oxide or to beyond 50mmHg (Nettina, 2006). Practically, a diagnosis of respiratory failure is made in clinical presentation and arterial blood gas analysis. A fall arterial oxygen tension (Pa,O2) of 6.0 kPa (45 mmHg) or both, is indicative of respiratory failure (Roussos and Koutsoukou, 2003). Respiratory failure may be acute or chronic. In case of Wilson, the respiratory failure is acute and this is indicated by the drastic change in the acid-base status (pH= 7.3). The cause of respiratory failure in him is the right lower lobe collapse-consolidation secondary to pneumonia. Lower respiratory tract infection is known as pneumonia. The pathology lies in the parenchyma of the lungs which consist of alveolar sacs. There are several causes to pneumonia, the most common of which is bacterial (Stephen, 2009). Bacterial pneumonia can be community acquired or hospital acquired. In case of Wilson, the pneumonia is hospital acquired. The most common respiratory failure is acute hypoxemic respiratory failure or type-1 which is seen in pneumonia. In acute respiratory failure, the pH is less than 7.3 (Nettina, 2009) as in Wilson. Decreased oxygen saturation: Acute respiratory failure occurs when the body is unable to maintain gas exchage at a rate on par with the demands of the body like in paneumonia. The damage to lung parenchyma in pneumonia results in release of inflammatory mediators and fluids because of which intrapulmonary shunting, ventilation-perfusion mismatching, hypoventilation and diffusion defects occur (Stephen, 2009). All these eventually lead to hypoxemia which is evident in the blood gas analysis of Wilson (Ranjit, 2001). In ventilation-perfusion mismatch, areas which have lower ventilation as against perfusion contribute to hypoxemia. Intrapulmonary shunt causes deoxygenated blood to bypass ventilation in the alveoli resulting in venous admixture of blood (Roussos and Koutsoukou, 2003). Both these mechanisms cause a widening in the alveolar-arterial oxygen difference. The normal difference is less than 15mmHg and when the difference exceeds this value, respiratory failure ensues (Kaynar and Sharma, 2009). The hypoxemia causes increased work of breathing resulting in respiratory fatigue. Respiratory fatigue and reduced alveolar ventilation in turn cause hypercarbia (Roussos and Koutsoukou, 2003).Thus, Wilson developed hospital-aquired pneumonia because of which adequate gas exchange commensurate with the needs of the body was not met, resulting in acute hypoxemic respiratory failure. Elevated respiratory rate and work of breathing: Increased respiratory rate and accessory muscle usage are indicators of increased work of breathing (Stephen, 2009), secondary to decreased oxygen in the blood. Respiratory acidosis: The hypoxemia causes increased work of breathing resulting in respiratory fatigue. Respiratory fatigue and reduced alveolar ventilation inturn causes hypercarbia (Roussos and Koutsoukou, 2003). Auscultation: Pneumonia occurs secondary to immune and inflammatory response secondary to bacteria. Due to this, fluid and pus accumulate in the airspaces. This is heard as crepitations on auscultation. The accumulation of pus causes collapse of the lungs causes decrease in air entry. Question-2 Antimicrobial agents are very essential for the management of hospital-acquired pneumonia. The most common cause of hospital acquired pneumonia is gram negative bacteria (Zang et al, 2007, Cochrane database). According to a study by Soo Hoo, Wen, Nguyen et al (2005), vancomycin with imipenem-cilastin-based regimen is superior to vancomycin with cefotaxime, ceftazidime or piperacillin based regimens as far as treatment of severe hospital acquired pneumonia is concerned. Masterton, Galloway, French et al (2009) opined that the choice of initial empirical antibiotic therapy must be based on the knowledge of the susceptibility patterns and nature of the pathogens prevalent in the individual unit and on other variables like comorbidities, duration of stay in the hospital and recent antibiotic therapy. Thus in Wilson, a two drug regimen must be initiated for antimicrobial management of pneumonia, based on the susceptibility patterns of the pathogens in the unit. Initially, vancomycin with imipenem-cilastin may be started until the culture reports are available. These drugs are broad spectrum antibiotics and can cover all potential organisms, both gram positive and gram negative. Once the organism is isolated, more specfic treatment can be instituted. Question-3 The two main nursing interventions essential for Wilson are improving gas exchange and pain management. Intervention-1 Improving gas exchange Wilson is conscious and alert (GCS-15) but has tachycardia (Heart rate-108 per minute), hypertension (Blood pressure- 165/98 mmHg), tachypnea (Respiratory rate- 28 per minute) and oxygen saturations of 89 percent on 6 liters per minute of oxygen via Hudson mask. He has hypoxemia (PaO2 58mmHg) and Hypercarbia (PaCO2 54mmHg). These findings are suggestive of acute respiratory failure secondary to pneumonia. The most important intervention necessary for Wilson is improvement of gas exchange. Gas exchange can be improved by administering antibiotics to resolve pneumonia; providing oxygen as needed, monitoring appropriate fluid balance by measuring intake and output, daily weight and urine specific gravity; preventing atelectasis by promoting chest expansion and secretion clearance with spirometry, nebulization and head end elevation; and monitoring the adequacy of ventilation using arterial blood gas analysis, vital capacity, respiratory rate and inspiratory force and by monitoring the need for mechanical ventilation. Oxygen therapy is life-saving in acute respiratory failure (Nettina, 2006) which Wilson is suffering from. Oxygen is essential for the tissues for survival and delivery of oxygen to the tissues in the body is dependent on ventilation, gas exchange, and circulatory distribution. In acute respiratory failure, secondary to pneumonia, tissue hypoxia occurs secondary to inadequate ventilation and inappropriate gas exchange (Ranji, 2001). The goal in oxygen therapy is to increase the saturation to more than 90 percent so that proper tissue oxygenation ensues (Ranjit, 2001 and Zang et al, 2007). Oxygen therapy in pneumonia is indicated when respiratory rate is more than 30 per minute or when there is acute respiratory failure or when the oxygen saturation is less than 92 percent (Zang et al, 2007). In Wilson, all these 3 findings are present and thus oxygen therapy is indicated. It is very important to initiate oxygen therapy because research has shown that "mortality from pneumonia has been shown to be related to arterial blood oxygen saturation" (Onyango, 1993; cited in Zang et al, 2007). In Wilson, the respiratory rate is 28 per minute, oxygen saturation is 89 percent and arterial blood gas analysis is suggestive of acute respiratory failure. Hence oxygen therapy is indicated in him. Oxygen may be delivered by low volume systems or high volume systems. The low volume systems are shields, nasal cannulae and masks. Side effects to these systems are discomfort, dryness of nasal mucosae and eyes and skin irritation. Delivery of oxygen is dependent on the ability of the patient to breathe. If low volume systems do not help in oxygenation, then high volume systems like non-invasive positive pressure ventilation, invasive positive pressure ventilation and continuous positive airway pressure or CPAPmust be employed for adequate oxygenation and ventilation of the patient. Wilson needs to be monitored every hours for improvement in respiratory rate and other vital signs, blood gas reports, oxygen saturations and level of consciousness. Failure to restore normal PaO2, PaCO2 and pH values of blood gas despite administration of antibiotics and oxygen therapy necessitates next level of oxygen therapy, CPAP. CPAP is a type of non-invasive ventilation which is designed to produce positive ventilation to the patient both during inspiration and expiration (Keen, 2000). It is a simple, yet gentle and inexpensive mode of respiratory system that helps prevent collapse of alveoli, thus increasing the functional residual capacity of lungs and reducing work of breathing (National Health Service, 2005). If Wilson is put on CPAP, he must be continuously monitored for level of conciseness, ABG and work of breathing. Deterioration in any of the 3 necessitates mechanical ventilation (National Health Service, 2005). The expected outcomes of this intervention are normal arterial blood gas analysis, decrease in respiratory rate, decrease in work of breathing and normal breath sounds in lung. Intervention-2 Reduction of pain In case of Wilson, the pain is due to fractured femur neck and subsequent open reduction and internal fixation. The type of pain is acute pain since it is sudden in onset (Wood, 2008)). Management of pain in the patient is very essential for holistic patient care. Pain management is also essential to treat respiratory failure. This is because increased pain caused increased respiratry rate and increased heart rate, thus causing increased consumption of oxyegen which is already compromised inWilson. Pain also causes inappropriate breathing patterns which do not optimise gas exchange. Another impotant reason why pain has to be managed is that pain causes anxiety which also increases respiratory rate and causes gas exchange compromise. The cornerstone for effective pain management is proper assessment which includes appropriate pain history, detailed physical examination and appropriate tests (Bird, 2005). There are several different tools to assess pain. On the 10 point scale, Wilson has pain of 5. But he insists on not taking morphine for pain because he thinks that he may get addicted to the drug. There are several medicines available to treat acute pain. The medicines must be prescribed as per the requirements of pain. The WHOs Pain Relief Ladder is a useful guide for nurses to prescribe pain-relief medications (WHO, 2009). The ladder has 3 steps of pain starting from below and moving upwards. The lowest step is that of mild pain. Mild pain is usually self-limited and may not require any treatment. The next step is that of moderate pain which is much severe than mild pain and affects functions of the patient. The pain disappears with treatment and seldom reappears. The uppermost step is that of severe pain which interferes with the functions of the patients and is a source of distress. According to WHO pain ladder (WHO, 2009), non-opioid medications like paracetamol and non-steroidal anti-inflammatory drugs like ibuprofen and aspirin are useful to manage mild pain. When the patient has moderate pain, the treatment must be stepped up to mild opioids like codeine. Further step in the management of pain would be stronger opiods like morphine, oxycodone, hydrocodone, methadone, hydromorphone and fetanyl. These medications must be provided until pain relief. Pain relief medication must be provided round the clock. In case of Wilson, the pain relief method is morphine through self-regulated PCA pump. This is not causing effcient pain relief because the patient is not taking enough medication because of fear of addiction. Hence it is very important for the nurse toWilson to take appropriate pain medication. Nurses have a major role in the diagnosis and management of pain in post-operative patients. They are the first persons to evaluate pain and thus are in a position to advise the treating doctor whether the pain remedy advocated was appropriate. Nurses can also evaluate the effects of the medications prescribed after the patient uses the medicines (Shaw, 2006). When a patient reports side effects, the nurse must record, manage and monitor the symptoms, guide physician about the condition of the patient and can suggest when to change the step in the analgesic ladder. Nurses have an important role in acting as coordinators of different specialities by educate the patients about the dosage of the drugs and about the need for good pain control (Delphi Study, 2007). According to the Medical Journal of Australia (Macintyre, Schug and Scott, 2006), opioids are the best medications to manage moderate to severe acute pain. Though no single opioid is superior to others, some opioids may be better in some patients. As far as respiratory depression is concerned, tramadol has the lowest risk of repertory depression (Macintyre et al, 2006). Nurses administering opioids for pain relief must use age as a predictor of opioid requirement than weight and must use sedation as an indicator for respiratory depression than decrease in respiratory rate. Common side effects for to opioids are constipation, nausea, somnolence. Other side effects which are dose-limiting are confusion, hyperalgesia, hallucinations, sedation and myoclonus. There are reports that switching to alternative opioid can reduce these symptoms (National Cancer Institute, 2009). The expected outcomes of this intervention are decreased respiratory rate, dcreased levels of anxiety, decrease in the oxygen supplement requirement and increase in oxygen saturation. References Bird, J. (2005). Assessing Pain in Older People. Nursing Standard, 19 (19), 45-52. Bateman, N.T., and Leach, R.M. (1998). Acute oxygen therapy. BMJ, 317, 798- 801. Delphi Study. (2007). WHO Normative Guidelines on Pain Management. Retrieved on 12th March, 2010 from http://72.14.235.132/search?q=cache:XaoHa1yWUgkJ:www.who.int/medicines/areas/quality_safety/delphi_study_pain_guidelines.pdf+Delphi+Study.+(2007).+WHO+Normative+Guidelines+on+Pain+Management&cd=1&hl=en&ct=clnk&gl=in Keen, A. (2000). Continuous positive airway pressure (CPAP) in the intensive care unit--uses and implications for nursing management. Nurs Crit Care., 5(3):137-41. Masterton, R.G., Galloway, A., French, G., et al. (2008). Guidelines for the management of hospital-acquired pneumonia in the UK: Report of the Working Party on Hospital-Acquired Pneumonia of the British Society for Antimicrobial Chemotherapy. Journal of Antimicrobial Chemotherapy, 62(1), 5-34. Macintyre, P.E., Schug, S.A., and Scott, D.A. (2006). Acute pain management: the evidence grows. The Medical Journal of Australia, 184(3), 101-102. National Cancer Institute. (2009). Pain. Retrieved on 12th March, 2010 from http://www.cancer.gov/cancertopics/pdq/supportivecare/pain/healthprofessional National Health Service. (2005). Guidelines for use fo CPAP systems in adults. Retrieved on 28th October, 2009 from http://www.ruh.nhs.uk/about/policies/documents/clinical_policies/blue_clinical/Blue_717_CPAP_Guidelines.pdf National Health Service Best Practice Statement. (2006). Management of chronic pain in adults. Retrieved on 12th March, 2010 from www.nhshealthquality.org Nettina, S.M. (2006). Manual of Nursing Practice. London: Lippincott, Williams and Williams. Ranjit. S. (2001). Acute respiratory failure and oxygen therapy. Indian J Pediatr., 68(3), 249-55. Roussos, C., and Koutsoukou, A. (2003). Respiratory failure. Eur Respir J Suppl., 47, 3s-14s. Regan, J.M. (2000). Neurophysiology of cancer pain. Medscape Pediatrics. Retrieved on 12th March, 2010 from http://www.medscape.com/viewarticle/408972 Shaw, S.M., (2006). Nursing & Supporting patients with chronic pain. Nursing Standard, 20(19), 60-65. Soo Hoo, G.W., Wen, Y.E., Nguyen, T.V., and Goetz, M.B. (2005). Impact of Clinical Guidelines in the Management of Severe Hospital-Acquired Pneumonia. 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