A 45-year-old male construction worker is diagnosed with ARDS and exhibits respiratory acidosis with significant hypoxemia. Which nursing intervention should be prioritized to improve the patient's oxygenation status?

B) Initiate non-invasive positive pressure ventilation (NIPPV) to enhance alveolar recruitment.

A) Administer intravenous fluids aggressively to improve renal perfusion.

B) Initiate non-invasive positive pressure ventilation (NIPPV) to enhance alveolar recruitment.

C) Position the patient in a high Fowler’s position to facilitate lung expansion.

D) Administer a bronchodilator to reduce airway resistance.

A 45-year-old male with ARDS presents with respiratory acidosis and significant hypoxemia. Based on the diagnostic findings and clinical priorities, which intervention should the nurse prioritize to improve the patient's oxygenation status?

B) Initiate non-invasive positive pressure ventilation (NIPPV).

A) Administer high-flow supplemental oxygen via nasal cannula.

B) Initiate non-invasive positive pressure ventilation (NIPPV).

C) Prepare the patient for immediate endotracheal intubation.

D) Increase the patient's IV fluid rate to enhance perfusion.

A patient with acute respiratory distress syndrome (ARDS) is experiencing worsening respiratory acidosis and hypoxemia despite high-flow nasal cannula therapy. Which nursing action is most appropriate to address the patient's deteriorating condition and prevent further organ dysfunction?

C) Prepare for intubation and mechanical ventilation.

A) Initiate prone positioning to improve oxygenation.

B) Administer a higher concentration of supplemental oxygen.

C) Prepare for intubation and mechanical ventilation.

D) Increase the flow rate on the high-flow nasal cannula.

A patient with worsening respiratory distress and hypoxemia is being considered for intubation and mechanical ventilation. Which of the following is the most appropriate initial action by the nurse to support this patient prior to the procedure?

D) Prepare the necessary equipment and notify the respiratory therapist.

A) Administer a sedative to reduce the patient's anxiety.

B) Elevate the head of the bed to improve ventilation.

C) Increase the FiO2 to 100% to maximize oxygenation.

D) Prepare the necessary equipment and notify the respiratory therapist.

A patient with ARDS on mechanical ventilation develops oliguria and rising serum creatinine levels. A bedside ultrasound shows a hyperdynamic heart with reduced preload. What is the most appropriate nursing intervention to address the patient's current condition?

D) Prepare to assist with vasopressor administration to support hemodynamics.

A) Administer a fluid bolus to improve renal perfusion.

B) Increase the FiO2 setting on the ventilator to improve oxygenation.

C) Administer a diuretic to reduce potential pulmonary edema.

D) Prepare to assist with vasopressor administration to support hemodynamics.

A patient with ARDS on mechanical ventilation is showing signs of acute kidney injury with oliguria and rising creatinine levels. A bedside ultrasound indicates reduced preload. Which nursing intervention is the most appropriate to address the patient's current hemodynamic status?

D) Request an order for vasopressors to maintain adequate mean arterial pressure without additional fluid administration.

A) Administer a diuretic to promote urine output and reduce potential fluid overload.

B) Increase the FiO2 on the ventilator to improve the patient's oxygenation status.

C) Initiate a fluid bolus to increase intravascular volume and improve renal perfusion.

D) Request an order for vasopressors to maintain adequate mean arterial pressure without additional fluid administration.

A patient with ARDS and concurrent renal dysfunction is receiving isotonic saline and low-dose norepinephrine to improve hemodynamic stability. Which assessment finding would indicate that the current treatment approach is effective?

A) Heart rate decreased to 80 bpm and blood pressure stabilized at 110/70 mmHg

B) Urine output decreased to 0.3 mL/kg/hr and blood pressure dropped to 85/55 mmHg

C) Respiratory rate increased to 30 breaths per minute and arterial pH decreased to 7.29

D) Serum creatinine increased to 2.5 mg/dL and lactate level rose to 4.0 mmol/L

A 65-year-old patient with ARDS and concurrent renal dysfunction shows an increase in serum creatinine and BUN, with arterial blood gas analysis indicating mixed respiratory and metabolic acidosis. After receiving a bolus of isotonic saline and low-dose norepinephrine, the patient's urine output improves slightly, but respiratory status remains critical. What is the nurse's priority intervention to support the patient's current treatment plan?

B) Collaborate with respiratory therapy to optimize ventilator settings.

A) Increase the rate of isotonic saline infusion to improve renal perfusion.

B) Collaborate with respiratory therapy to optimize ventilator settings.

C) Administer a diuretic to enhance urine output and relieve pulmonary edema.

D) Continue sedation to maintain patient comfort and prevent agitation.

A patient with ARDS is showing signs of worsening pulmonary edema and decreased renal function. The interdisciplinary team decides to adjust the fluid management strategy and ventilator settings. What is the most important nursing action to prioritize in monitoring this patient’s condition?

C) Track urine output hourly to evaluate renal function.

A) Monitor daily weights to assess fluid balance.

B) Regularly assess breath sounds for changes in respiratory status.

C) Track urine output hourly to evaluate renal function.

D) Check blood pressure every 4 hours to ensure hemodynamic stability.

A patient with ARDS is experiencing worsening lung compliance and signs of fluid overload, prompting adjustments in fluid management and ventilator settings. Which nursing intervention is most appropriate to evaluate the effectiveness of the new ventilator strategy?

A) Monitor the patient’s arterial blood gas results for improved oxygenation and reduced carbon dioxide levels.

B) Assess the patient's urine output to ensure adequate renal perfusion.

C) Measure the patient’s blood pressure to check for signs of hypotension.

D) Evaluate the patient’s skin turgor to assess for dehydration.

ARDS - Nursing Case Study

Pathophysiology

• Primary mechanism: In ARDS, an acute inflammatory response damages the alveolar-capillary membrane, leading to increased permeability. This results in protein-rich fluid leaking into the alveoli, causing pulmonary edema and impaired gas exchange.

• Secondary mechanism: The inflammatory process activates immune cells, releasing cytokines that exacerbate lung tissue injury and contribute to the formation of hyaline membranes, further disrupting alveolar function and reducing lung compliance.

• Key complication: The combination of edema and inflammation results in severe hypoxemia, as oxygen cannot efficiently diffuse into the bloodstream, leading to respiratory distress and potential multi-organ dysfunction if untreated.

Patient Profile

Demographics:

45-year-old male, construction worker

History:

• Key past medical history: Hypertension, Type 2 Diabetes

• Current medications: Lisinopril 20 mg daily, Metformin 1000 mg twice daily

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Difficulty breathing and persistent cough

• Key symptoms: Rapid breathing, chest pain, fatigue, low oxygen saturation

• Vital signs: Temperature 38.2°C, Heart rate 110 bpm, Respiratory rate 28 breaths per minute, Blood pressure 128/78 mmHg, Oxygen saturation 88% on room air

Section 1

New Diagnostic Results:

As the medical team continues to monitor the 45-year-old male construction worker with suspected ARDS, a series of diagnostic tests are performed to further evaluate his condition. The results of an arterial blood gas (ABG) analysis reveal a pH of 7.32, PaCO2 of 50 mmHg, and PaO2 of 55 mmHg, indicating respiratory acidosis with significant hypoxemia. A chest X-ray shows diffuse bilateral infiltrates consistent with pulmonary edema and likely ARDS, with a notable lack of cardiomegaly, helping to differentiate this from cardiogenic pulmonary edema. Additionally, a complete blood count (CBC) reveals leukocytosis with a white blood cell count of 15,000/µL, suggesting an ongoing inflammatory response or possible infection.

Concurrently, a basic metabolic panel indicates an elevated blood urea nitrogen (BUN) of 32 mg/dL and a creatinine level of 1.5 mg/dL, pointing towards potential renal involvement, possibly as a consequence of hypoperfusion secondary to hypoxemia. The elevated inflammatory markers and the presence of diffuse infiltrates corroborate the diagnosis of ARDS, but they also raise concerns about the risk of progression to multi-organ dysfunction syndrome (MODS) if the hypoxemia is not promptly addressed.

These findings require the healthcare team to engage in clinical reasoning to prioritize interventions aimed at improving oxygenation and preventing further complications. Initiating supplemental oxygen therapy and considering non-invasive positive pressure ventilation (NIPPV) or mechanical ventilation may be necessary to enhance alveolar recruitment and improve gas exchange. The team must also be vigilant in monitoring renal function and adjusting fluid management to prevent aggravating pulmonary edema while maintaining adequate organ perfusion. These considerations set the stage for the next steps in the patient's management and highlight the complexity of balancing respiratory support with overall organ function.

Section 2

Change in Patient Status:

Despite the initiation of supplemental oxygen therapy and the consideration of non-invasive positive pressure ventilation, the patient's oxygenation status continues to decline. Over the next several hours, his oxygen saturation drops to 85% on a high-flow nasal cannula delivering 60% FiO2. The patient begins to exhibit increasing respiratory distress, characterized by the use of accessory muscles and a respiratory rate elevated to 32 breaths per minute. His blood pressure remains relatively stable at 128/78 mmHg, but his heart rate has increased to 115 beats per minute, indicating a compensatory response to hypoxemia and possible early signs of systemic stress.

The nursing team notes a change in the patient's neurological status; he becomes increasingly lethargic and difficult to arouse, suggesting worsening hypoxemia and the potential onset of hypercapnic encephalopathy. A repeat arterial blood gas analysis reveals further deterioration with a pH of 7.28, PaCO2 of 58 mmHg, and PaO2 of 50 mmHg, confirming worsening respiratory acidosis and hypoxemia. These changes necessitate a critical reassessment of the current management plan, as the patient's condition suggests an urgent need for intubation and mechanical ventilation to provide adequate respiratory support and prevent further organ dysfunction.

In light of the patient's compromised status, the healthcare team must swiftly engage in clinical reasoning to balance the risks and benefits of mechanical ventilation. Consideration of lung-protective ventilation strategies, such as low tidal volume ventilation, is crucial to minimize the risk of ventilator-induced lung injury. The escalation of care prompts a multidisciplinary discussion to reassess fluid management strategies, ensuring that appropriate measures are in place to support renal function without exacerbating pulmonary edema. These developments highlight the complexity of managing ARDS and underscore the importance of timely interventions to stabilize the patient and prevent progression to multi-organ dysfunction syndrome.

Section 3

Following the decision to intubate and initiate mechanical ventilation, the patient is placed on a lung-protective ventilation strategy. The ventilator settings are adjusted to deliver low tidal volumes of 6 ml/kg of predicted body weight and maintain plateau pressures below 30 cm H2O to minimize the risk of ventilator-induced lung injury. This adjustment initially stabilizes the patient's respiratory status, as evidenced by a slight improvement in oxygen saturation to 92% on an FiO2 of 70%. However, the patient's respiratory distress remains significant, and there is a persistent requirement for sedation to ensure ventilator synchrony and comfort.

Despite these respiratory-focused interventions, new complications emerge. The patient develops oliguria, with urine output decreasing to less than 0.5 mL/kg/hr over the past four hours, indicating potential acute kidney injury. Laboratory results reveal elevated serum creatinine levels, rising from 1.0 mg/dL to 1.8 mg/dL, and an increase in blood urea nitrogen (BUN) from 20 mg/dL to 35 mg/dL, suggesting worsening renal function. This decline necessitates further evaluation of the patient's fluid balance and renal perfusion. The healthcare team must deliberate the judicious use of diuretics versus potential fluid resuscitation, weighing the risks of exacerbating pulmonary edema against the need to support renal function.

The patient's evolving condition prompts a comprehensive review of his hemodynamic status. A focused bedside ultrasound is performed, revealing a hyperdynamic heart with evidence of reduced preload, consistent with potential intravascular volume depletion. These findings prompt a careful reassessment of fluid management strategies, considering the use of vasopressors to maintain adequate mean arterial pressure while avoiding excessive fluid administration. The interdisciplinary team, including nephrology and critical care specialists, collaborates to refine the treatment plan, aiming to stabilize renal function while continuing to optimize respiratory support. This complex interplay of organ systems exemplifies the challenges of managing ARDS with multi-organ involvement and underscores the importance of vigilant monitoring and adaptive clinical reasoning.

Section 4

In light of the patient's evolving condition, the interdisciplinary team decides to perform a comprehensive reassessment of the patient's hemodynamic and renal status, focusing on new diagnostic results to guide further management. Laboratory tests are repeated, revealing a further increase in serum creatinine to 2.2 mg/dL and BUN rising to 42 mg/dL, confirming ongoing renal impairment. Concurrently, arterial blood gas analysis shows a pH of 7.31, PaCO2 of 48 mmHg, and HCO3 of 22 mEq/L, indicating a mixed respiratory and metabolic acidosis. The patient's lactate level is also elevated at 3.5 mmol/L, suggesting hypoperfusion and potential tissue hypoxia.

These findings prompt the team to adjust the treatment strategy. Given the evidence of intravascular volume depletion from the bedside ultrasound, a decision is made to cautiously administer a bolus of isotonic saline while closely monitoring for any signs of fluid overload that could exacerbate pulmonary edema. At the same time, low-dose norepinephrine is initiated to support the mean arterial pressure, aiming to improve renal perfusion without compromising respiratory function. The patient's vital signs are monitored meticulously, with blood pressure stabilizing at 90/60 mmHg and heart rate at 110 bpm, reflecting a more favorable hemodynamic profile.

As the team implements these interventions, the patient's response is closely observed. Within the next few hours, urine output shows a slight improvement, increasing to 0.6 mL/kg/hr, and there is a modest improvement in the patient's acid-base balance, with a pH rising to 7.35. However, the patient's respiratory status remains tenuous, with continued reliance on mechanical ventilation and high levels of sedation. These developments highlight the delicate balance required in managing ARDS with concurrent renal dysfunction, emphasizing the need for ongoing multidisciplinary collaboration and vigilant reassessment to adapt the treatment plan as the patient's condition evolves.

Section 5

As the day progresses, the interdisciplinary team continues to monitor the patient closely, given the known risks associated with ARDS and the recent interventions. Despite initial improvements in hemodynamic stability and acid-base balance, the patient's condition takes a concerning turn. The respiratory therapist notes increased resistance in the ventilator, suggesting possible worsening lung compliance. A repeat chest X-ray reveals new bilateral infiltrates, indicative of progressing pulmonary edema. This prompts a reassessment of the patient's fluid status and ventilatory settings.

In light of these changes, the team re-evaluates the fluid management strategy. The decision is made to reduce the rate of isotonic saline infusion and increase the diuretic therapy to mitigate fluid overload. Concurrently, adjustments are made to the ventilator settings to optimize oxygenation without causing barotrauma, transitioning to a high-frequency oscillatory ventilation mode. These modifications aim to alleviate the mechanical burden on the lungs while continuing to support adequate gas exchange.

Meanwhile, laboratory results return showing a further rise in creatinine to 2.5 mg/dL, compounded by a drop in urine output to 0.4 mL/kg/hr, indicating worsening renal function. This compels the nephrology team to consider renal replacement therapy options, weighing the risks and benefits given the patient's fragile state. As these developments unfold, the team remains vigilant, understanding that the patient's path is precarious and requires continuous reassessment and adaptive management to navigate the challenges of ARDS amid evolving complications.