Reflective Analysis of Viva Voce

Introduction

Viva voce and a reflection, both a requirement for successful completion of the course. For somebody not used to this form of assessment process, it is just but normal to ask oneself what? , why? and how?. Although a brief and complete orientation, description and information was provided in the early part 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 able 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 appreciation (Mann et al. 2009).

Description

This 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. X’s 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 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 output and high Systemic Vascular Resistance (SVR) as a result of hypovolaemia. It can be due to excessive fluid loss such as haemorrhage, vomiting, diarrhoea, burns or inadequate fluid intake (Adam and Osborne, 2005).

Strengths and Areas for Development

Stress 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 conceived about. In the end, the anticipation 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 along the way but acceptable although can be overall improve given the situation.

Upon presentation of Mr. X’s assessment details and laboratory result, and concluded hypovolaemia as a cause of haemodynamic compromise based 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 active bleeding. During my discussion, I have mentioned about how low circulating blood volume results in decrease End Diastolic Volume (EDV). This stimulates the baroreceptors located at the aortic arch and carotid sinuses to send signal to the medullary centre of the brain which 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.

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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 stimulated because of decrease renal blood flow , which in turn is converted 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 water 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 free 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 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 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 importantly, to continue to look after haemodynamically compromised patients to help facilitate maintain and improve a level of my competency and skills in Intensive care nursing.

Implication for Practice

With 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 standard of care through mentorship.

References

Adam, 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/1º e 2º Ciclos – Lics e Lics com Mests/MD/1ºANO/2ºSEM/12-UBA5/TPs/TP1/Baynes Cap11- Metabolismo da Glucose.pdf [Accessed12/12/13]

Jevon, P. and Ewens, B. (2008) Monitoring of the Critically Ill Patient. Second Edition. Oxford: Blackwell Publishing

Kelly, D. M. (2005) Critical Care Nursing. Volume 28, no. 1 pp 2-19. Lippincott. Williams and Williams, inc.

Gunnerson, K et al. (2013) Lactic Acidosis[online] Available from: http://emedicine.medscape.com/article/167027-overview [Accessed12/12/13]

Mann, 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/s10459-007-9090-2

McGloin, S. and McLeod, A. (2010) Advance Practice in Critical Care – A Case Study Approach. Oxford. Blackwell Publishing

Appendix 1

On 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 sedation 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, proceeded with extubation at 20:30. His risk factors are; prev. MI, HTN, DM type 2, high Cholesterol, smoker and TIA x2. At 22:00 his assessment findings are:

HR 110- 120 bpm

BP 85/55 mmhg

MAP 55-60 mmhg

CVP 2

Temp. 36.5

Urine output 25mls/ hr ( Weighs 85kg)

GCS : E4V4M6

Mediatinal drain 25mls –serosanguineous

Bloods:

K+ 4.9 mmol/L

Na 143 mmol/L

Urea 8 mmol/L

Creatinine 80 umol/L

Hb. 9.0 g/L

Hct 35%

WBC 8.4 k/ul

ABG’s

pH 7.29

pCO2 5.54 kPa

pO2 18.4 kPa

HCO3 19.4 mmol/L

BE -5.9 mmol/L

Lactate 1.9 mmol/L

He 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.