Reflective Analysis of Viva Voce

Reflective Analysis of Viva VoceIntroductionViva voce and a reflection, both a requirement for successful completion of the course. For somebody not utilise to this form of assessment process, it is just but traffic pattern to ask oneself what? , why? and how?. Although a brief and complete orientation, description and information was provided in the early go of the curriculum, it is only in the end that I have fully understand its significance to my learning. Through the viva voce and a reflective writing that I was qualified to evaluate myself in terms of what I have learned? (Knowledge), what I can do? (Skills gained), and what I have become? (Attitude) A competent practitioner. A highlight that I have to address in the Intensive Care Course. For it is in a reflective practise that we gain new understanding and grip (Mann et al. 2009).DescriptionThis is a reflective piece about my viva voce that revolves around my care of a 73 year old male 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 physiological compensatory mechanism involve and the care given.Review of Mr. X history sheet and assessment details found in appendix 1, was suggestive of hypovolaemic 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 output and high Systemic Vascular Resistance (SVR) as a resultant role of hypovolaemia. It can be due to excessive still loss such as haemorrhage, vomiting, diarrhoea, burns or inadequate fluid intake (Adam and Osborne, 2005).Strengths and Areas for DevelopmentStress and anxiety, is always a major predicament that I had been most worried about. I have tried to alleviate this from reading, rehearsing and any other form of preparation needed one would have con ceived about. In the end, the expectancy that your next, was the most gruelling.I believe, I was in its entirety at best well prepared, organized and chronological in my presentation of points and information with some hiccups on the way but acceptable although can be overall improve given the situation.Upon presentation of Mr. Xs assessment details and laboratory result, and conclude hypovolaemia as a cause of haemodynamic compromise standstilld 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 circulating blood volume. His Haemoglobin level was acceptable and there is no signs of progressive bleeding. During my discussion, I have mentioned about how low circulating blood volume results in decrease End Diastolic ledger (EDV). This stimulates the baroreceptors located at the aortic arch and carotid sinuses to send signal to the myelinery centre of the brain whi ch in turn causes the release of adrenalin 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 establish haemostasis. In renal response I have mentioned the involvement of the Renin Angiotensin Aldosterone System. Not to be exhaustive with information, this involves the release of renin through the action of the juxtaglomerular cells turned on(p) because of decrease renal blood flow , which in turn is reborn to angiotensin 1 by angiotensinogen. Angiotensin 1 is then transformed 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 peeing retention. A surge in osmolarity in the blood stimulates the release of Antidiuretic hormone (ADH) or vasopressin from the posterior pituitary gland. This results in the reabsorption of solute justify water in the distal tubules and collecting 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 satisfied 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 anaerobic 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 product referred to as pyruvate, a three carbon acid. Inside the cell with mitochondria and oxidative metabolism, this is converted completely into Co2 and water known as aerobic glycolysis (Baynes, n.d.). In contrary, lactic acid is the end product of anaerobic breakdown of glucose in the tissues during dogged 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 increasing pattern with a base excess noted at 5.9.Familiarity and consistency in my opinion is my area of development. I need to continually update myself with the ever changing needs of the client more so, of the profession. This includes current research based guidelines and policies. From reading books, journals, articles, new discoveries or trends in the field of critical care. more than importantly, to continue to look after haemodynamically compromised patients to facilitate facilitate maintain and improve a level of my competenc y and skills in Intensive care nursing.Implication for PracticeWith the knowledge and skills that I have gained from the viva voce and looking 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 doing so. With the knowledge and skills that I will be bringing back to the unit, I will be able to help enhance the received of care through mentorship.ReferencesAdam, S. K. and Osbourne, S. (2005) Critical Care Nursing Science and Practice. Second Edition. Oxford Oxford University Press.Baynes, J. W. (n.d.) Anaerobic Metabolism of Glucose in the Red Blood Cells online Available 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- Metabolismo da Glucose.pdf Accessed12/ 12/13Jevon, P. and Ewens, B. (2008) Monitoring of the Critically Ill Patient. Second Edition. Oxford Blackwell PublishingKelly, 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 magisterial 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 Case Study Approach. Oxford. Blackwell PublishingAppendix 1On the start of the shift , received a patient in ITU who is 73 years of age, now 6 hours post CABG. He has been weaned off drugging and now ready for extubation. Pre operatively his echo showed good LV. Upon review of his chart showed a blood pressure of 140/60 mmhg. Now fully awake, procee ded with extubation at 2030. His risk factors are prev. MI, HTN, DM type 2, high Cholesterol, smoker and TIA x2. At 2200 his assessment findings areHR 110- 120 metronome markingBP 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/LUrea 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.