Advanced Respiratory and Hemodynamic Management in Critical Care NUR4020

Q1a. Lung Protective Ventilation Strategy

Mr. Stewart has pulmonary contusion and hemopneumothorax, so he requires LPV and prevention of VILI. This strategy uses low VT ranging from 46 mL/kg of predicted body weight to minimize barotrauma and volutrauma which are devastating especially to compromised lungs with low compliance (Nguyen et al., 2021). Mr. Stewart confirmed there is pulmonary contusion which implies that his lung compliance is reduced, therefore, his lungs are stiffer and more prone to over-expansion if greater tidal volumes are given. PEEP should be carefully ruled up to the levels, that provide enough oxygenation (PaO2 > 60 mmHg or SpO2 > 90%), at the same time, preventing alveolar overdistention due to pulmonary contusions and atelectasis caused by hemopneumothorax (Mourad & Rose, 2020).
PCV is preferred for Mr. Stewart because it restricts the peak airway pressures and maintains the pressure to a gentle and continuous pattern which subsequently decreases the chances of barotrauma. Reactive management in this way is useful given chest wall injury, and significantly reduced compliance. In addition, increasing the respiratory rate aids in the removal of CO2 and corrects hypercapnia, but should not be done to the extent of causing auto-PEEP and dynamic hyperinflation which in turn worsens VILI (Tsonas et al., 2022). The factors that contribute to Mr. Stewarts respiratory failure are V/Q imbalance, shunt within the lung, and diffusion limitation. V/Q mismatch results from lung consolidation and/or collapse, intra-pulmonary shunt occurs when blood is diverted to lungs segments that receive little or no ventilation, and alteration in diffusion capacity results from hemorrhagic infiltration of the alveolar-capillary membrane due to contusions (Slobod et al., 2022).

Q1b. Interpretation of Mr. Stewarts (ABG)

Mr. Stewarts arterial blood gas (ABG) analysis reveals a pH of 7.30, while high reflecting acidaemia; a PaO2 of 69 mmHg and SaO2 of 89% leads to hypoxemia; a PaCO2 of 79 mmHg was high indicating hypercapnia though the HCO3- was normal at 24 mmol/L. These factors are V/Q mismatch, intrapulmonary shunting, and diffusion impairment that could explain hypoxemia in the patient. This leads to V/Q imbalance, which occurs in the areas of lung collapse and consolidation due to the occurrence of pulmonary contusions and hemopneumothorax (Mourad & Rose, 2020; Slobod et al., 2022).

Hypercapnia identified in the case of Mr. Stewart points to hypoventilation which is a result of reduced lung compliance caused by pulmonary contusions and rib fractures that enhance the work of breathing and decrease the efficiency of ventilation. Knowing that pH equals 7. 30 patients, with elevated PaCO2 while HCO3- remains normal, it can be concluded that there is an acute form of respiratory acidosis with no sign of metabolic compensation mostly indicating acute form. Research evidence LPV strategies with low VT and adequate PEEP lowered the mortality rate in ARDS and other acute lung conditions due to a reduction in overdistension and alveolar collapse that leads to VILI (Nguyen et al., 2021). It is important in the traumatized patient alarm to note that hypoxemia and hypercapnia management through ventilation methods are strategic in patients with poor respiratory mechanics (Tsonas et al., 2022).

Q2a. Strategies to Reduce the Risk of (VAP)

1. Elevate the Head of the Bed:

Simple interventions such as elevating the head of the bed at 30-45 degrees reduces the occurrences of aspiration which is a leading cause of VAP with Mr. Stewart. This position reduces the occurrence of aspiration pneumonia since it minimizes the chance of gastric fluids regurgitating into the lungs (Gner & Kutlutrkan, 2021).

2. Implement an Oral Care Protocol with Chlorhexidine:
Through proper dental care and the use of chlorhexidine antiseptic in specific cases, the amount of dental plaque containing respiratory pathogens can be minimized. An effective oral care protocol that is carried out every 4 hours contributes to reducing bacterial count within the oropharynx and thus the chances of these bacteria being aspirated to the lower respiratory tract (Brookes et al., 2020).

3. Use Subglottic Secretion Drainage:
Subglottic secretion drainage entails the use of endotracheal tubes that has an additional channel above the cuff to aspirate subglottically either continuously or intermittently any secretions that may have formed in the subglottic space. These washings lessen the likelihood of these secretions to be aspirated distal to the cuff which is traditionally how VAP occurs (Chair et al., 2020).

Q2b. Rationale for Each Strategy

1. Raising the head of the bed can avoid aspiration through application of gravity to fight progression of stomach content to the lower respiratory area. Gner and Kutlutrkan (2021), reported that these incidences were lower in patients positioned at 45 degrees as compared to those lying flat.

2. Chlorhexidine mouthwash rinse decreases the density of bacteria within the oropharynx area, which is an essential factor in the occurrence of VAP. Medjedovic et al. (2023) conducted a study with evidence showing that chlorhexidine mouthwash oral care was effective in the prevention of VAP among the mechanically ventilated patient population.

3. Chair et al. (2020), through their study, concluded that subglottic secretion drainage tended to result in a low incidence of VAP. This strategy is specifically useful in ensuring that there is no obstruction in the airway and no colonization of bacteria.

Q3: Inotrope choice for Mr Stewart

Due to Mr. Stewarts hemodynamic instability, including the blood pressure of 90/55 mmHg, MAP 62, and CVP 10mmHg in this case, norepinephrine is suitable for inotropic therapy (Yu et al., 2023). Norepinephrine is an ardent vasoconstrictor that works on alpha- & beta-adrenergic receptors to optimize hypotensive issues primarily in septic and hypovolemic shock (Hamzaoui & Shi, 2020).

Norepinephrine mainly acts on alpha-1 receptors to cause marked vasoconstriction, and therefore a rise in SVR is also observed. This effect raises the blood pressure essential for Mr. Stewart as his MAP is significantly low. Thus, by raising perfusion pressure, norepinephrine helps to maintain the necessary blood supply to the organs (Hamzaoui & Shi, 2020). Intramuscularly administered norepinephrine also has a mediocre beta-1-adrenergic effect that may facilitate myocardial contractility and increase cardiac output. This mild inotropic effect is used with advantage regarding Mr. Stewart because although he was effectively resuscitated with fluids, his blood pressure is reduced (Hamzaoui & Shi, 2020). Increased CO will aid the improvement of tissue perfusion and oxygen supply. Thus, by raising the MAP, norepinephrine ensures the perfusion of organs with end products to the vital and necessary organs including the brain, kidneys, and cardiac tissue to prevent end-organ damage to Mr. Stewart, who is a critically ill patient and is prone to develop multi-organ failure due to prolonged hypotension (Yu et al., 2023).

Norepinephrine is preferred as a first choice of vasopressor in septic and hypovolemic shock because it raises BP and perfusion fairly well and does not seem to be very deadly. Such investigations have revealed that the use of norepinephrine in critically ill patients with shock has a better rate of survival as compared to other drugs of its class (Hamzaoui & Shi, 2020). Russell et al. (2020) illustrated that the primary choice of vasopressor in shock management is norepinephrine. Norepinephrine effectively attenuates hypotension and reduces mortality in the critical care patients without raising the risk of arrhythmias unlike dopamine inotropes.

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