Reflective Analysis of Viva Voce

Reflective Analysis of oral examination VoceIntroductionViva voce and a reflection, both a requirement for successful completion of the course. For someone not used to this pull in of assessment process, it is just but shape to ask oneself what? , wherefore? and how?. Although a brief and complete orientation, description and training was provided in the early part of the curriculum, it is only in the end that I have fully understand its signifi poopce to my learning. Through the viva voce and a reflective writing that I was fitting to evaluate myself in term of what I have learned? (K directlyledge), what I can do? (Skills gained), and what I have become? (Attitude) A competent practitioner. A toweringlight that I have to address in the Intensive Care Course. For it is in a reflective practise that we gain new understanding and appreciation (Mann et al. 2009). commentaryThis is a reflective piece about my viva voce that revolves around my electric charge of a 73 year old m ale referred to as Mr X, 6 hours post Coronary Artery Bypass Graft. As he became hemodynamically compromised, I have discussed Mr. Xs assessment in relation to a normal physiologic compensatory mechanism involve and the sell given.Review of Mr. X history sheet and assessment details found in addendum 1, was suggestive of hypovolemic shock as further supported by his clinical symptoms. Clinically, it can be classified as mild, moderate or severe (Kelly, 2005).This leads to organ hypoperfusion characterized by tachycardia, hypotension, oliguria, decrease cardiac return and high Systemic Vascular Resistance (SVR) as a result of hypovolaemia. It can be callable to excessive fluid loss such as haemorrhage, vomiting, diarrhoea, burns or inadequate fluid intake (Adam and Osborne, 2005).Strengths and Areas for Development attempt and anxiety, is always a major predicament that I had been close to disordered about. I have tried to alleviate this from reading, rehearsing and any other f orm of preparation needed one would have conceived about. In the end, the anticipation that your next, was the most gruelling.I believe, I was in its entirety at best swell prepared, organized and chronological in my presentation of points and information with some hiccups on the way but acceptable although can be overall repair given the situation.Upon presentation of Mr. Xs assessment details and lab result, and concluded hypovolaemia as a cause of haemodynamic compromise ground on supporting evidences, I, at some point, preceded in the discussion of physiological responses as a result of decrease in cardiac output. This is due to decrease in circulate occupation volume. His Haemoglobin level was acceptable and there is no signs of active bleeding. During my discussion, I have mentioned about how secondary circulating blood volume results in decrease End diastolic Volume (EDV). This stimulates the baroreceptors located at the aortic arch and carotid sinuses to displace s ignal to the medullary centre of the brain which in turn causes the forgo of ad nephriticin and noradrenalin by the action of the adrenal medulla (Jevon and Evens, 2008). This supported why Mr. X is tachycardic.The human body compensates in various ways through the involvement of different organ system working together to confirm haemostasis. In renal response I have mentioned the involvement of the Renin angiotonin Aldosterone System. Not to be exhaustive with information, this involves the release of renin through the action of the juxtaglomerular cells touched because of decrease renal blood flow , which in turn is reborn to angiotensin 1 by angiotensinogen. Angiotensin 1 is then modify by the Angiotensin Converting Enzyme (ACE) predominantly found in the lungs to Angiotensin II, a potent vasoconstrictor. Furthermore, the release of aldosterone from the adrenal cortex causes increase in renal sodium and water retention. A surge in osmolarity in the blood stimulates the rel ease of Antidiuretic hormone (ADH) or vasopressin from the posterior pituitary gland. This results in the reabsorption of solute free water in the distal tubules and store system of the kidneys and further stimulates peripheral vasoconstriction (McGloin and McLeod, 2010). With the reabsorption of sodium and water, coupled with vasoconstriction the circulating blood volume is improved thus, result in the increase in the end diastolic volume. This improves muscle contraction of the heart and overall the cardiac output. Hence Mr. X low urine output.Although I felt cheery about my presentation of cardiac and renal responses to a decrease in cardiac output, my explanation in regards to metabolic acidosis more specifically in the aspect of cellular an oxidative metabolism was somehow lacking in its content.Glucose being a major carbohydrate, is a fuel used by cells in our body. Its metabolism travels through a pathway called glycolysis with the end output referred to as pyruvate, a th ree carbon acid. Inside the cell with mitochondria and aerophilous metabolism, this is converted completely into Co2 and water k promptlyn as aerobic glycolysis (Baynes, n.d.). In contrary, lactic acid is the end product of anaerobic segmentation of glucose in the tissues during persistent oxygen deprivation secondary to an insult caused by decrease circulating blood volume, and owerwhelming of the bodies buffering abilities (Gunnerson et. al. 2013). These explains why Mr. X lactate shows an increase pattern with a base excess noted at 5.9.Familiarity and torso in my opinion is my area of development. I need to continually modify myself with the ever changing needs of the client more so, of the profession. This includes current seek based guidelines and policies. From reading books, journals, articles, new discoveries or trends in the field of minute care. much importantly, to continue to look after haemodynamically compromised patients to help facilitate proceed and improv e a level of my competency and skills in Intensive care nursing.Implication for PracticeWith the knowledge and skills that I have gained from the viva voce and feel after clients with haemodynamic instability, supported with theory during lectures and mentoring, I am better able to understand what is happening inside the body as is tries to compensates to maintain haemostasis. More importantly, act upon the needs of the patient, and anticipates interventions with rationales for insideng so. With the knowledge and skills that I will be deliverance back to the unit, I will be able to help upgrade the standard of care through mentorship.ReferencesAdam, S. K. and Osbourne, S. (2005) Critical Care Nursing acquirement and Practice. Second Edition. Oxford Oxford University Press.Baynes, J. W. (n.d.) Anaerobic Metabolism of Glucose in the Red Blood Cells online open from http//molar.crb.ucp.pt/cursos/1 e 2 Ciclos Lics e Lics com Mests/MD/1ANO/2SEM/12-UBA5/TPs/TP1/Baynes Cap11- Metabol ismo da Glucose.pdf Accessed12/12/13Jevon, P. and Ewens, B. (2008) Monitoring of the Critically Ill Patient. Second Edition. Oxford Blackwell publicationKelly, D. M. (2005) Critical Care Nursing. Volume 28, no. 1 pp 2-19. Lippincott. Williams and Williams, inc.Gunnerson, K et al. (2013) lactic Acidosisonline Available from http//emedicine.medscape.com/article/167027-overview Accessed12/12/13Mann, K., Gordon, J. MacLeod, A. (2009) Reflection and reflective practice in health professions education a systematic review. Adv Health Sci Educ Theory Practice, 14(4), 595-621. doi 10.1007/s10459-007-9090-2McGloin, S. and McLeod, A. (2010) Advance Practice in Critical Care A eccentric person Study Approach. Oxford. Blackwell PublishingAppendix 1On the start of the free , received a patient in ITU who is 73 years of age, now 6 hours post CABG. He has been weaned off sedation and now ready for extubation. Pre operatively his echo showed good LV. Upon review of his chart showed a blood press ure of 140/60 mmhg. Now fully awake, proceeded with extubation at 2030. His risk factors are prev. MI, HTN, DM type 2, high Cholesterol, tobacco user and TIA x2. At 2200 his assessment findings areHR 110- great hundred bpmBP 85/55 mmhgMAP 55-60 mmhgCVP 2Temp. 36.5Urine output 25mls/ hr ( Weighs 85kg)GCS E4V4M6Mediatinal drain 25mls serosanguineousBloodsK+ 4.9 mmol/LNa 143 mmol/Lcarbamide 8 mmol/LCreatinine 80 umol/LHb. 9.0 g/LHct 35%WBC 8.4 k/ulABGspH 7.29pCO2 5.54 kPapO2 18.4 kPaHCO3 19.4 mmol/LBE -5.9 mmol/LLactate 1.9 mmol/LHe is on maintenance fluids of 85ml/hour 5% Dextrose, 2L of geloplasma cautiously given against CVP and eventually started on Noradrenaline to achieve a MAP of 70mmhg.