Viva voce and critical reflection are both a prerequisite for a successful completion of the intensive care course. Hence, for someone not used to being assessed in this form, it would be considered normal to ask oneself what? why? and how? Although a complete explanation, description and information was provided both in the early part and at the end of the curriculum in addition to a one-to-one conversation with the course lead, it is only at the end that I fully understood its importance to my learning and practice. The viva voce and a reflective writing availed me the opportunity to critically evaluate myself with reference to the knowledge and skills I have acquired, and my development as a competent critical care nurse. Which is in line with Koshy et al., 2017, who say that through good reflective practice we develop our self, become better leaners as we gain new understanding and appreciation.
This is a reflective essay about my viva voce that revolves around my care of a 54-year-old lady referred to as Ms H, 12 days since transfer to the intensive care unit for increasing oxygen requirement after testing positive for Covid -19 post- operatively following a right Knee replacement. As her respiratory requirements increased, I have discussed Mr. X’s assessment in relation to normal pathophysiological response and acceptable supportive treatments involved and the care given.
Review of Ms. H’s current clinical status and assessment details found in appendix 1, was suggestive of acute respiratory distress syndrome (ARDS) as further supported by her clinical symptoms. This leads to non-cardiogenic pulmonary oedema characterized by refractory hypoxemia on pulse oximeter and arterial blood gas (ABG), bilateral lung infiltrates in the absence of increased capillary hydrostatic pressure, increased work of breathing and respiratory rate. It can be due to direct or indirect injury to the lungs (Clark and Soos, 2021).
Currently, clinically there are no biomarker molecules that are useful in the prediction of the severity of ARDS. However, using the arterial oxygen partial pressure (PaO2 in mmHg) to fractional inspired oxygen (FiO2) ratio (P/F) with a positive end expiratory pressure of >5cmH2O, it can be classified as mild, moderate, or severe (ARDS Definition Task Force et al., 2012).
Viva voce is an examination method which I have never had the experience of, hence, naturally, I was most concerned about the expectations and process. In addition to this, stress, and anxiety, was a major predicament that I was most worried about, which was compounded by my fear of my possibly undiagnosed aphasia which at times is profound during any talking related communication. I tried alleviating this by reading, rehearsing, and recreating what I thought as a near similar situation as the viva voce. In the end, the anticipation that it is time, was the most gruelling.
Strengths and Areas for Development
I believe, I was in its entirety at best the most prepared, organized and chronological in my presentation of points and information with some hiccups along the way but acceptable although can be improved overall given the situation.
Upon presentation of Ms. H’s assessment details and laboratory result and concluding with direct lung injury by Covid-19 pneumonitis resulted in ARDS as a cause of worsening refractory hypoxemia despite optimal FiO2 supply as supported by the clinical evidence such the chest x-ray (CXR), and physical examination. I, at some point, with some prompt by direct question from the assessor, preceded in the discussion of the pathophysiology of the syndrome and the physiological responses as a result of supportive treatment.
During my discussion, I stated how this insult to Ms. H’s respiratory system manifests as a range of pathophysiological presentations leading to her clinical signs and symptoms. There are three identified phases of ARDS. The exudative phase which is seen in days 1-7. The proliferative phase seen from around day 7, and the fibrotic phase which if patient gets to, is generally seen around 2-3 weeks after the initial onset (Choi, 2010, Aokage, et al, 2015)
In the exudative phase the normal alveoli and capillary membrane is disrupted, which leads to a disruption of ventilation and oxygenation. This disruption is due to the activation of the resident macrophages, the inflammatory signally cascades of pro-inflammatory cytokines (Butt, et al, 2016). This inflammation causes damage to the endothelium leading to an influx of protein rich fluid into the alveoli due to increased permeability of the membrane (Drahnak and Custer, 2016). As a result of the loss of the oncotic pressure favouring fluid resorption, more fluid can permeate and flood the lungs, resulting in alveolar and interstitial oedema (Sinha and Bos, 2021). Aokage et al. (2015) says that the resulting impedance in the production of surfactant due to the influx of fluid makes way for the fibrin and plasma proteins to develop hyaline membrane on the alveolar walls which can impede gas exchange and decrease lung compliance due to atelectasis (Sinha and Bos, 2021). The resulting effect of atelectasis is the continued evident refractory hypoxemia. This is notable in Ms H’s clinical presentation as there is the need to use a higher set inspiratory pressure to generate a volume of 390ml. In addition, despite ventilation at a 100% FiO2 the PaO2 falls below the normal range.
The proliferative phase is characterised by continued inflammation of the endothelium and epithelium (Aokage et al., 2015). There is further decrease in lung compliance due to more profound atelectasis as a result of further damage to the alveoli cells that make surfactants causing a decreased production of surfactant (Drahnak and Custer, 2015). According to Butt, Kurdowska and Allen (2016) as the proliferative phase continues there is organised fibrosis as a result of granulation tissue.
In the third and final phase of the ARDS process known as the fibrotic stage, there is chronic inflammation. Interstitial fibrosis and continues proliferation of the alveolar cells (Choi, 2010).
Furthermore, in my discussion, using my calculation of her P/F ratio of 45mmHg, I showed that she fell into the category of severe ARDS. This is also supported by the difference between her alveola (A) and arterial (a) concentration of oxygen (A-a gradient) which is widened at 610 showing ventilation/perfusion mismatch (V/Q) (Sarkar, Niranjan and Banyal, 2017). V/Q mismatch occurs when one or more areas of the lung either receive oxygen but no blood flow or vice versa, thus not partaking in gas exchange. However, as her hypoxemia is not corrected with the FiO2, it is apparent that she developed right-to-left shunt (Patel, Lazdunski and Honore, 1997 cited by Sarkar, Niranjan and Banyal, 2017). This happens when blood form the right part of the heart enters the left without partaking in gas exchange due to in this case the fluid and exudate filled alveoli and atelectasis.
Following this, I also explained the rationale for choosing inverse ratio of inspiratory time to expiratory time ventilation as a supportive treatment to improve ventilation through longer inspiratory time.
When asked to explain Ms H’s ABG, I was able to explain that the acid-base disturbance was metabolic alkalosis as evinced by the elevated bicarbonate and base excess.
Although I felt somewhat satisfied with my presentation of pathophysiology of ARDS, I found my self short in my ability to name the alveolar type 1(AT1) cell and alveolar type11 (AT11) cells in the alveoli when asked. The AT1 is a thin cell layer lining the alveolar epithelium that permits gas exchange, while the AT11 produce surfactants that permits lung expansion (Matthay et al., 2019). In addition, though I was able to explain the phases and severity of ARDS, I was disappointed in my inability to link it to the Berlin 2012 definition of ARDS and the rationale behind the consensus.
Furthermore, although I could name and explain some alternative supportive intervention for ARDS such as proning which aids a more evenly distributed lung perfusion due to gravity and improves V/Q in addition to recruitment of atelectatic lungs (McCormack and Tolhurst-Cleaver, 2017). I could not exhaustively talk above extracorporeal membrane oxygenation (ECMO) and I found myself lacking in my knowledge of the mechanism of inhaled nitric oxide (iNO) which is an inhaled gas with high affinity for oxyhaemoglobin. Due to its unique ability to induce pulmonary vasodilation in areas of the lung with adequate ventilation, it improves oxygenation of blood and decreases right to left shunt. In their randomised placebo-controlled trial, Dowell, Thomas and Yehya (2017) found that the early use of iNO reduced the average number of days that mechanical ventilation was required by paediatric patients. Likewise, Albert et al. (2017) in their pilot study found that iNO improved oxygenation significantly in adults. Although, the articles I read infer that there is no evidence of its improvement in mortality, the existing research show a favourable efficacy in early use.
At the end of my viva when asked what infusion could be adding to the alkalosis, though I said the loop diuretic, rather that say Furosemide I mention potassium, which impacted on my ability to explain that as a result of the inhibition of the sodium-potassium-chloride cotransporter, reabsorption of sodium and chloride is inhibited leading to the excretion of sodium, chloride and hydrogen ions resulting in the accumulation of bicarbonate (Klabunde, 2017).
With the knowledge, skills, and self-awareness gained from the viva voce and looking after patients with ARDS, supported with taught theory during lectures, mentoring and independent reading, I am better able to understand what is happening inside the body as it tries to respond to an insult to the lungs. More importantly, the need for identification of ARDS and early interventions of supportive treatment with rationale for doing so. With the knowledge and skills that I will be bringing back to my unit, I will be able to help enhance the standard of care through mentorship.