Acute Care Nursing

Introduction To Case Bill Type 2 Diabetes Case Study

The 75 year old patient Bill who had been earlier diagnosed with Type 2 Diabetes. For about thirty Five Years, Bill has smoked a pack of cigarette each day along with the history of heavy alcohol use too. He did quit after he was being diagnosed a year back for Diabetes. Bill has started with mertformin 500 mg, to be had twice a day and is oral prescription. The dosage was increased to 1000 mg twice a day. The latest HbA1C level is 7.2%. The fasting glucose has varied between 4,5 – 7 mmol/L. The glucose control has been fluctuating to a greater extent and has not stabilized. The History that Bill has is that mother was diabetic and did die of cardiac arrest at the age of 65. Bill runs juice bar and is fond of fresh fruits. He consumes a banana each day and has a sedentary lifestyle. The visit last week at a General Practitioner got a BP reading of 170/100 mmHg. He did not have any symptoms associated with headache, dizziness or blurred vision. Although Bill did complain of the discomfort in the eyes wherein the eyes are feeling tired. Considering the physical examination of Bill, he weighs 123 Kgs and is 175 cm tall.

The resting pulse rate in case of Bill is 82 over minute. The RR is 18 and temperature 37 degrees. The physical system examination showed remarkable condition. The lesions on the nail and skin are not present but the presence of pitting oedema in both the lower legs is present. The increased protein level in urine is concerning. The Level of Urea has also increased with the examination of the Blood Report of Bill. The reading of Serum Albumin is 6.1 mg/dl and there is reduced Estimated Glomerular Filtration Rate. The 24 hour urine test reveals the higher than the normal range excretion of Albumin for Bill. Bill returns home after staying in the hospital for 5 days. He has been feeling fatigued and is also depressed about the current health status. The has been drinking two large glasses of wine in the evenings for past two days post his discharge.

The epigastric pain is what Bill felt one day while he was asleep. This event took place at 2 AM. The pain did not even subside in the morning until 5 AM and intensified into the jaw and the left shoulder. Then Bill drove to the ED. With the crushing pain experienced in heart for Bill, he had the nausea and the diaphoresis too. The ECG is being taken and the blood work reveals the enhanced level of cardiac Troponin T and Creatine Kinase. Considering the case it is significant to draw upon the Pathophysiology of Acute Cardiac event Bill does experience.

Pathophysiology of Acute Cardiac Event

The cardiac event is the cessation of the cardiac mechanical activity which results in the absence of blood circulation. The cardiac event will stop the blood to flow to the vital organs in the body (Morgan et al., 2017; Reis et al., 2017; Myerburg, 2017; Uchino et al., 2016; Sekhon et al., 2017). The organs will deprive of the oxygen levels. In the case, while this is untreated, the result of death can be very well considered. The sudden cardiac event is the unexpected cessation with respect to the blood circulation taking place within the shortest possible time span. This can even take place without any warning.

The sudden cardiac event does tend to occur outside the hospitals and just in US alone, the mortality is 90%. The sudden cardiac event is considered to be the commonest cause of death considering the global status (Morgan et al., 2017; Reis et al., 2017; Myerburg, 2017; Uchino et al., 2016; Sekhon et al., 2017). The categorization pertains to as to where they take pace. The management of cardiac events is significant and at the same time challenging too and the impact is felt on the kidney, brain and the heart.

In case of Bill, the pathophysiology of acute cardiac event takes into consideration the understanding of such an event (Morgan et al., 2017; Reis et al., 2017; Myerburg, 2017; Uchino et al., 2016; Sekhon et al., 2017). The focus is primarily on the acute and decompensated cardiac failure rather than being the vascular failure. The cause is associated to the chronic disease. Bill is already having the chronic disease (Morgan et al., 2017; Reis et al., 2017; Myerburg, 2017; Uchino et al., 2016; Sekhon et al., 2017). He is diagnosed with Type 2 Diabetes. The fluid overload considering the cardiac event takes into account the symptoms associated with the congestion and the normalization.

The cardiac arrest can lead to the global ischemia condition wherein the consequence is at the cellular levels and impacts the functionality of the organ. The consequences are significant as the cellular damage and the oedema formation are crucial. The oedema is harmful to the brain (Morgan et al., 2017; Reis et al., 2017; Myerburg, 2017; Uchino et al., 2016; Sekhon et al., 2017). There is minimum room for the brain to expand. This does lead to the increased intracranial pressures being built up and the decrease in the cerebral perfusion post resuscitation.

The short term along with the lon term cerebral dysfunction is significant. This does tend to bring about the altered state of alertness and can also involve seizures. The decrease in the levels of adenosine triphosphate (ATP) production results in the loss of membrane with the efflux taking place, that od the potassium (Morgan et al., 2017; Reis et al., 2017; Myerburg, 2017; Uchino et al., 2016; Sekhon et al., 2017). The influx of the calcium and the sodium is present. The excess of sodium results in the cellular oedema. The excess levels of calcium tend to damage the mitochondria and the increased levels of nitric oxide production takes place (Morgan et al., 2017; Reis et al., 2017; Myerburg, 2017; Uchino et al., 2016; Sekhon et al., 2017). The same results in the activation of the proteases which results in the further damage to the cells. The abnormal ion flux does tend to result in the depolarization of the neurons. This releases the neurotransmitters and some of the neurotransmitters are damaging to a greater extent.

The glutamate activates the specific calcium channel and worsens the intracellular calcium overload. The inflammatory mediators too are elaborated and result in the microvascular thrombosis along with the loss of vascular integrity (Morgan et al., 2017; Reis et al., 2017; Myerburg, 2017; Uchino et al., 2016; Sekhon et al., 2017). This results in enhanced oedema formation. The mediators tend to trigger the apoptosis which can rest in the accelerated death of the cells.

Analysis of Immediate Management Approaches

It is crucial to consider the immediate management approaches – Both medical and nursing in case of Bill with an acute cardiac condition. Considering the medical management, the ECG depicts the image of Bill’s heart and the areas identified wherein the heart has been damaged and not pumping the blood causing pressure upon the valves (Moskowitz et al., 2018; Morgan et al., 2017; Juvé-Udina, et al., 2017; Moulaert et al., 2016; Harrison & Merchant, 2018; Guetterman et al., 2018). The anti-arrhythmic drug ( Flecanide | Amiodarone | Lidocaine (through IV) ) are essential. The complications can be more for Bill and the medications would need to be continued for a longer duration.

For the nursing management, based upon the Coronary Bypass Surgery for Bill due to the congestion, the sewing of the veins or the arteries in place would need to be carried out. The restoration of the blood flow to the narrowed or the blocked arteries would be significant (Moskowitz et al., 2018; Morgan et al., 2017; Juvé-Udina, et al., 2017; Moulaert et al., 2016; Harrison & Merchant, 2018; Guetterman et al., 2018). The blood supply would need to be improved in case of Bill. Post the surgery the nursing management would also stand to be crucial. The aspects of postoperative and preoperative nursing need to be taken into consideration. The monitoring has to be done very closely of the pulmonary status and the maintenance of airway patency. The report or any changes in case of pulmonary congestion, dyspnoea or the SPO2 going below a 92% is crucial and the weaning protocols would need to be taken into consideration (Moskowitz et al., 2018; Morgan et al., 2017; Juvé-Udina, et al., 2017; Moulaert et al., 2016; Harrison & Merchant, 2018; Guetterman et al., 2018). The monitoring of the vital signs in the nursing is significant. The record intake and the output per hour needs to be monitored. The monitoring of the clarity and the colour of the urine too would form to be significant part of the nursing intervention undertaken.

The renal perfusion if any needs to be immediately notified to the surgeon. The assessment of Bill’s cardiac status and hemodynamic status needs to be done and well monitored. The nursing intervention would also include the complication of Atrial Fibrillation which can complicate the case of Bill (Moskowitz et al., 2018; Morgan et al., 2017; Juvé-Udina, et al., 2017; Moulaert et al., 2016; Harrison & Merchant, 2018; Guetterman et al., 2018). The complication arising due to post cardiac surgery, it can even be life threatening. The mediation or the synchronized cardioversion would need to be arranged for Bill. The assessments – Peripheral and the Neurovascular would stand to be crucial (Boyce & Gossens, 2017). The assessment would need to be strictly monitored for the first eight hours. The stability of Bill’s condition would need to be taken into consideration.

The checks would need to be performed every two hours and every hours for the following 8 hours (Moskowitz et al., 2018; Morgan et al., 2017; Juvé-Udina, et al., 2017; Moulaert et al., 2016; Harrison & Merchant, 2018; Guetterman et al., 2018). The neurological status of Bill needs to be gauged as well. As Bill is already having kidney problems too due to the level of cardiac Troponin T and Creatine Kinase, the care post-surgery stands to be significant.

References for Bill Type 2 Diabetes Case Study

Boyce, L. W., & Goossens, P. H. (2017, February). Rehabilitation after cardiac arrest: integration of neurologic and cardiac rehabilitation. In Seminars in neurology (Vol. 37, No. 01, pp. 094-102). Thieme Medical Publishers.

Guetterman, T. C., Kellenberg, J., Krein, S., Lehrich, J., Harrod, M., Kronick, S., ... & Nallamothu, B. K. (2018). Nursing roles for in-hospital cardiac arrest response: a qualitative study. Circulation, 138(Suppl_2), A180-A180.

Harrison, J. M., & Merchant, R. M. (2018). Leveraging the Healthcare Workforce to Improve Outcomes for Survivors of Cardiac Arrest.

Juvé-Udina, M. E., Fabrellas-Padrés, N., Adamuz-Tomás, J., Cadenas-González, S., Gonzalez-Samartino, M., Ariza, C., & Delgado-Hito, P. (2017). Surveillance nursing diagnoses, ongoing assessment and outcomes on in-patients who suffered a cardiorespiratory arrest. Revista da Escola de Enfermagem da USP, 51.

Kragholm, K., Wissenberg, M., Mortensen, R. N., Hansen, S. M., Malta Hansen, C., Thorsteinsson, K., ... & Køber, L. (2017). Bystander efforts and 1-year outcomes in out-of-hospital cardiac arrest. New England Journal of Medicine376(18), 1737-1747.

Moulaert, V. R., Goossens, M., Heijnders, I. L., Verbunt, J. A., & van Heugten, C. M. (2016). Early neurologically focused follow-up after cardiac arrest is cost-effective: A trial-based economic evaluation. Resuscitation, 106, 30-36.

Morgan, R. W., Fitzgerald, J. C., Weiss, S. L., Nadkarni, V. M., Sutton, R. M., & Berg, R. A. (2017). Sepsis-associated in-hospital cardiac arrest: epidemiology, pathophysiology, and potential therapies. Journal of critical care, 40, 128-135.

Moskowitz, A., Berg, K. M., Grossestreuer, A. V., Cocchi, M. N., Sarge, J., Williams, D., ... & Donnino, M. W. (2018). Cardiac Arrest in the Intensive Care Unit: A Preventable Problem. Circulation, 138(Suppl_2), A266-A266.

Myerburg, R. J. (2017). Sudden cardiac death: interface between pathophysiology and epidemiology. Cardiac electrophysiology clinics, 9(4), 515-524.

Reis, C., Akyol, O., Araujo, C., Huang, L., Enkhjargal, B., Malaguit, J., ... & Zhang, J. H. (2017). Pathophysiology and the monitoring methods for cardiac arrest associated brain injury. International journal of molecular sciences, 18(1), 129.

Sekhon, M. S., Ainslie, P. N., & Griesdale, D. E. (2017). Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model. Critical Care, 21(1), 90.

Uchino, H., Ogihara, Y., Fukui, H., Chijiiwa, M., Sekine, S., Hara, N., & Elmér, E. (2016). RETRACTED ARTICLE: Brain injury following cardiac arrest: pathophysiology for neurocritical care. Journal of intensive care, 4(1), 31.

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