CASE STUDY 1
Explain the pathogenesis causing clinical manifestation with which Mrs. Brown is presented.
According to Mrs. Brown’s case, her clinical manifestation suggeststhat she is experiencing acute exacerbation of chronic obstructivepulmonary disease (COPD). Coccia,Palkowski, Schweitzer Motsohi, & Ntusi, 2015),assert that dyspnea is a symptom of either congestive heart failureor chronic obstructive pulmonary disease. Acute dyspnea varies widelyamong individuals who are exposed to similar pathologies. Normally,it is a complex symptom that emanates from psychological damage andalarms one to the hypothesis of the jeopardized homeostasis. Thebreathing discomfort mainly happens as a result of eithercardiovascular or via media of respiratory system, but in some cases,it may also be assigned to metabolic derangements, and neuromuscularconditions (Coccia et al., 2015). According to the clinicalmanifestation in Mrs. Brown’s case, dyspnea originates either fromasthma or cardiac origin, pneumonia, and psychogenic disorders(Gudder et al., 2014).
According to Gudder et al. (2014), heart failure is the endstage of all diseases that affects the heart and it is one of theleading causes of sickness and death. It can be defined as theinability of the heart to pump enough blood to the body. The Bloodpressure of Mrs. Brown is higher than the normal rate of 120/80mm Hg.In this case, Mrs. Brown present stage 2 Hypertension and her heartpumps blood at high rate against the artery walls. This might be asresult of heart failure and the inability of the body to pump normalblood to the body. However, in Mrs. Brown’s case, ChronicObstructive Pulmonary Disease is the persistence limitation ofairflow that is progressive over time (Gudder et al., 2014).Mrs. Brown is complaining of severe shortness of breath, which isaccompanied by high heart beat rate. According to her clinicalmanifestations, she is having 110 beats per minute that is higherthan the normal heart beat rate between 60-100 beats per minute. Thissituation is referred to as tachycardia due to the fact that herheart struggles to deliver more oxygen and energy for the bodyactivity at rest. This is a common problematic aspect of theclinician-patient interface because articulating patient’shistorical experience might be complicated. It happens because of themanifestation of the biological, social, and psychological challengesthat an individual face as noted by Coccia et al. (2015).
Heart failure and COPD is as a consequence of exposure to harmfulstimuli that frequently emanates from smoking tobacco. The standardincendiary response is amplified in the individuals prone to COPDdevelopment (Shapiro and Ingenito, 2016). Shapiro and Ingenitofurther emphasize that the current description of COPD includeschanges to a great and small airways and alveolar space. Smallairways changes may cause excess luminal edema, and cellularinfiltration (2016). Therefore, elastolysis may lead to loss ofalveolar attachment with airways distortion and be narrowing of COPD(Shapiro and Ingenito, 2016). Similarly, they further posit thatsmall airway impedimenta together with wall inspissation and presenceof inflammatory mucous oozes and the CD8 T cell inflammation arelinked with COPD and advancing of the disease.
Heart failure is a common primary disease of the elderly because ofthe untimely organ maturing with unfathomed systematic effect and thechronic progressive course that affect vastly on health-relatedquality of life and exercise permissiveness. In this case, Mrs. Brownis an individual with a history of heart failure and her condition isperceived as an increased respiratory of work that brought on bypulmonary ventilation not matching the drive to breathe. Her severeshortness of breathing is associated with respiration of 25 breathsper minute. This shows that her respiration rate is a little high atrest. Mrs. Brown’s SpO2 is 85% that constitute a normal oxygensaturation for a normal average adult at room air. According toCoccia et al. (2015), is a dissociation among pulmonaryventilation and respiratory drives from the unsuitable match betweenafferent receptors in the airways, chest wall structures, centralrespiratory motor activities, and lungs. The psychological pathwayswill ultimately contribute to shortness of breath through particularacid-sensing ion channels, mechanoreceptors, and long receptors. Thiscondition is associated with the auscultation crackles at the base ofthe lung.
Mrs. Brown was connected to ECG that recorded whether or not herheart is functioning normally. However, the ECG presented artificialfibrillation that is a common condition among individual with heartfailure. Artificial fibrillation is also present in patient whoexperience severe shortness of breath/dyspnea. The performance of theECG was to identify the artificial fibrillation as a symptom andmanaging it through the control of the arrhythmia or diagnosis ofheart failure as presented in Mrs. Brown’s case.
Discuss two high priority nursing strategies to manage and provide evidence-rationales for those strategies
Nursing care for a patient like Mrs. Brown, who is an individual withCOPD and experiences severe dyspnea should seek early recognition ofexacerbation to prevent frequent hospitalization and possible acuteheart failure (O’Donnell et al., 2008 cited in Bailey et al.,2010). This is a primary strategy because it demands strong knowledgeand understanding of the symptoms reflective of severe exacerbationconsequences. A nurse should use detailed assessment that includesonset questions, frequency, intensity as well as the nature of therespiratory change. Therefore, coming up with processes of reviewingand maintaining consistent approaches to treatment across the contextwill assist nurse’s capacity to teach and re-enforce patient’sdisease and management strategies.
Secondly, another nursing strategy should involve early screening forMrs. Brown because she has a history of heart failure. This isimportant in the sense that Mrs. Brown’s family did not rendermanifest confirming mass screening of the patient. Likewise, thisstrategy is essential because the nurse providing care for Mrs. Brownwill be able to enforce or carry out appropriate nursinginterventions for all levels of dyspnea including the acute sequencesof respiratory distress. On the other hand, the use ofimmediate-release oral is another intervention that is effective inMrs. Brown’s case. It will help the patient to reduce theventilator requirement by cutting down central respiratory demand(Bailey et al., 2010).
Bailey, H.,Bartlett, A., Beatty, G., Bissonnette, J., Debrowsky B., Manji, M.,McMillan, C., Pallock, R., and Santos, J. (2010). Nursing Care ofDyspnea: The 6thVital Sign in Individuals with Chronic Obstructive Pulmonary Disease(COPD) 2010 Revised. NursingBest Practice Guideline.
Coccia, C.,Palkowski, G., Schweitzer, B., Motsohi, T., & Ntusi, N. (2015).Dyspnoea: Pathophysiology and a clinical approach. SouthAfrican Medical Journal, 106(1),32-36. doi:10.7196/SAMJ.2016.v106i1.10324
Gudder, G., Brenner, S., Stork, S., Hoes, A., and Rutten, F. (2014).Chronic Obstructive Pulmonary Disease in Heart Failure: AccurateDiagnosis and Treatment. European Journal of Heart Failure, 16,1273-1282, doi:10.1002/ejhf.183
O’Donnell, D. E., Aaron, S., Bourbeau, J., Hernandez, A.,Marciniuk, D. D, Balter, M. et al. (2008). Canadian ThoracicSociety recommendations for management of chronic obstructivepulmonary disease- 2008 update. Canadian Respiratory Journal,(Suppl A), 1A-8A.
Shapiro, S.and Ingnito, E. (2016). The Pathogenesis of Chronic ObstructivePulmonary Disease. Pulmonary and Critical CareMedicine, Harvard Medical School, Boston, Massachusetts.