A patient with a diagnosis of cor pulmonale and severe pulmonary hypertension is being treated with high-flow nasal cannula oxygen therapy, intravenous diuretics, and a low-dose beta-blocker. Considering the patient's current condition and treatment regimen, which nursing intervention is the highest priority?

B) Assess the patient's respiratory rate and effort to detect signs of worsening respiratory failure.

A) Monitor serum potassium levels closely and administer potassium supplements as needed.

B) Assess the patient's respiratory rate and effort to detect signs of worsening respiratory failure.

C) Initiate infection control precautions to prevent nosocomial infections.

D) Educate the patient about the importance of adhering to a low-sodium diet to manage heart failure symptoms.

A patient with cor pulmonale, severe pulmonary hypertension, and an acute exacerbation of a chronic respiratory condition is being treated with high-flow nasal cannula (HFNC) oxygen therapy, intravenous diuretics, and a low-dose beta-blocker. Considering the patient's current clinical status, which nursing intervention is the highest priority to prevent further clinical deterioration?

B) Adjust the high-flow nasal cannula settings to maintain a PaO2 above 60 mmHg and reduce work of breathing.

A) Monitor the patient’s electrolyte levels closely, especially potassium, to prevent cardiac arrhythmias.

B) Adjust the high-flow nasal cannula settings to maintain a PaO2 above 60 mmHg and reduce work of breathing.

C) Initiate continuous cardiac monitoring to detect any arrhythmias due to potential electrolyte imbalances.

D) Assess the patient's response to diuretics by monitoring urinary output and signs of fluid overload.

A patient with acute respiratory distress is showing signs of severe respiratory acidosis and hypoxemia despite high-flow oxygen. After initiating non-invasive ventilation, the healthcare team considers further interventions. Which of the following should be prioritized to address the patient's condition and prevent further deterioration?

B) Perform a therapeutic thoracentesis to relieve the pleural effusion and improve respiratory function.

A) Administer potassium replacement to correct hypokalemia and prevent cardiac arrhythmias.

B) Perform a therapeutic thoracentesis to relieve the pleural effusion and improve respiratory function.

C) Initiate broad-spectrum antibiotics to address the possibility of underlying sepsis.

D) Increase the flow rate of oxygen delivery to maximize oxygen saturation levels.

A patient with a history of right-sided pleural effusion and worsening respiratory status is being treated with non-invasive ventilation and broad-spectrum antibiotics. Despite high-flow nasal cannula support, the patient's oxygen saturation remains critically low at 82%, and arterial blood gas analysis indicates severe respiratory acidosis and hypoxemia. What should be the nurse's priority intervention to address the patient's immediate respiratory needs?

B) Prepare for intubation and mechanical ventilation

A) Increase the FiO2 on the non-invasive ventilator to 100%

B) Prepare for intubation and mechanical ventilation

C) Administer a bronchodilator to alleviate wheezing

A patient with suspected septic shock and acute kidney injury (AKI) on non-invasive ventilation presents with hypokalemia, declining renal function, and a risk of fluid overload. Which intervention should the nurse prioritize to stabilize the patient's condition while minimizing potential complications?

B) Initiate continuous renal replacement therapy (CRRT) to manage fluid balance and support kidney function.

A) Administer a potassium-sparing diuretic to address hypokalemia and fluid overload.

B) Initiate continuous renal replacement therapy (CRRT) to manage fluid balance and support kidney function.

C) Increase intravenous fluid administration to maintain adequate blood pressure and perfusion.

D) Adjust antibiotic therapy to narrow-spectrum agents based on culture results.

A patient with a suspected septic shock and acute kidney injury (AKI) following therapeutic thoracentesis presents with persistent hypotension, rising creatinine levels, and reduced urine output. Considering the complex interplay of fluid management, infection control, and potential electrolyte imbalances, which of the following nursing interventions is the most appropriate to prioritize at this time?

C) Titrate vasopressor support to maintain a mean arterial pressure (MAP) above 65 mmHg.

A) Administer a bolus of 500 mL normal saline to improve perfusion despite the risk of fluid overload.

B) Initiate continuous renal replacement therapy (CRRT) to manage acute kidney injury and fluid balance.

C) Titrate vasopressor support to maintain a mean arterial pressure (MAP) above 65 mmHg.

D) Administer potassium supplementation to address hypokalemia and prevent arrhythmias.

A patient with altered mental status has been found to have a critically low potassium level of 2.8 mEq/L and a serum sodium level of 131 mEq/L. The healthcare team is implementing a potassium replacement protocol while monitoring the patient's cardiac status. What is the most appropriate nursing intervention to prioritize during the potassium replacement therapy?

B) Monitor the patient's cardiac rhythm continuously and assess for signs of arrhythmias during potassium replacement.

A) Administer potassium chloride intravenously as a rapid bolus to quickly correct hypokalemia.

B) Monitor the patient's cardiac rhythm continuously and assess for signs of arrhythmias during potassium replacement.

C) Restrict the patient's fluid intake to prevent further dilution of serum sodium levels.

D) Schedule a repeat CT scan to reassess for any delayed intracranial changes post electrolyte correction.

A patient with acute kidney injury presents with confusion, agitation, and a recent drop in the Glasgow Coma Scale score. A CT scan rules out intracranial pathology, and laboratory results show hypokalemia and hyponatremia. Which nursing intervention should be prioritized to address the patient's condition and prevent further complications?

C) Implement continuous cardiac monitoring and cautiously replace potassium

A) Administer intravenous potassium chloride rapidly to correct hypokalemia

B) Initiate fluid restriction to manage hyponatremia

C) Implement continuous cardiac monitoring and cautiously replace potassium

D) Administer hypertonic saline to increase serum sodium levels quickly

A patient with acute kidney injury and hypokalemia is receiving intravenous potassium replacement. The healthcare team notices premature ventricular contractions (PVCs) and mild peripheral edema. Which intervention should the nurse prioritize to ensure the patient's safety and stability?

C) Collaborate with the healthcare team to initiate a diuretic therapy while monitoring electrolyte levels closely.

A) Administer additional potassium to correct the hypokalemia more rapidly.

B) Increase the rate of intravenous fluids to enhance renal perfusion and prevent further kidney damage.

C) Collaborate with the healthcare team to initiate a diuretic therapy while monitoring electrolyte levels closely.

D) Discontinue cardiac monitoring since the patient is showing neurological improvement.

A patient with acute kidney injury is receiving intravenous potassium supplementation due to hypokalemia and is being monitored for potential complications. After noting premature ventricular contractions (PVCs) on the cardiac monitor, the nurse observes mild peripheral edema. Based on these findings, what is the nurse's best action?

B) Notify the healthcare provider and discuss the potential need for adjusting the diuretic regimen.

A) Increase the rate of potassium infusion to quickly correct the hypokalemia.

B) Notify the healthcare provider and discuss the potential need for adjusting the diuretic regimen.

C) Reduce the oxygen flow rate to decrease fluid retention.

D) Discontinue the potassium infusion immediately to prevent cardiac complications.

CARDIOPULMONARY - Nursing Case Study

Pathophysiology

• Primary mechanism: Pulmonary hypertension leads to increased pressure in the pulmonary arteries, causing right ventricular hypertrophy and eventually right-sided heart failure as the heart struggles to pump against elevated resistance.

• Secondary mechanism: Ventilation-perfusion mismatch in lung disease reduces oxygen delivery to tissues, exacerbating hypoxemia and increasing cardiac workload due to compensatory mechanisms like tachycardia.

• Key complication: Chronic hypoxia and pressure overload can cause cor pulmonale, where the right side heart failure progresses, leading to systemic venous congestion, peripheral edema, and organ dysfunction.

Patient Profile

Demographics:

68-year-old male, retired coal miner

History:

• Key past medical history: Chronic obstructive pulmonary disease (COPD), coronary artery disease, type 2 diabetes mellitus, hypertension, history of smoking (40 pack-years)

• Current medications: Albuterol inhaler, Lisinopril, Metformin, Atorvastatin, Aspirin, Tiotropium

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Severe shortness of breath and chest pain

• Key symptoms: Persistent cough with sputum, cyanosis, fatigue, palpitations, peripheral edema, orthopnea

• Vital signs: Blood pressure 88/56 mmHg, heart rate 132 bpm, respiratory rate 28 breaths per minute, temperature 101.4°F, oxygen saturation 82% on room air

Section 1

As the healthcare team continues to manage the patient's condition, new diagnostic results provide critical insights into the underlying pathology. An echocardiogram reveals significant right ventricular hypertrophy and dilation, confirming the presence of cor pulmonale. The estimated right ventricular systolic pressure is markedly elevated at 65 mmHg, indicating severe pulmonary hypertension. A subsequent arterial blood gas analysis shows a pH of 7.32, PaCO2 of 58 mmHg, and PaO2 of 48 mmHg, reflecting a state of acute respiratory acidosis superimposed on chronic hypoxemia. These findings suggest an acute exacerbation of his chronic respiratory condition, likely triggered by a concomitant infection or progression of his pulmonary disease.

Moreover, a comprehensive metabolic panel highlights a serum potassium level of 3.0 mEq/L, indicating hypokalemia, which could be exacerbating his cardiac arrhythmias and contributing to his palpitations. His B-type natriuretic peptide (BNP) is significantly elevated at 1,200 pg/mL, consistent with the degree of heart failure. A chest X-ray reveals pulmonary congestion and prominent pulmonary arteries, along with a right-sided pleural effusion, further complicating his respiratory status. These findings underscore the need for aggressive management of both his cardiac and respiratory conditions.

In response to these results, the clinical team initiates a multifaceted treatment strategy. Oxygen therapy is escalated to high-flow nasal cannula to improve his oxygenation status. Intravenous diuretics are administered cautiously to address the fluid overload while monitoring for electrolyte imbalances. The patient is started on a low-dose beta-blocker to manage his tachycardia and improve cardiac output, despite the challenges posed by his COPD. An infectious disease workup is underway to rule out any underlying infection, given his elevated temperature and respiratory symptoms. The healthcare team remains vigilant for potential new complications, such as worsening respiratory failure or arrhythmias, as they continue to reassess and adjust the treatment plan accordingly.

Section 2

As the clinical team closely monitors the patient's progress, a sudden change in his status prompts immediate attention. During a routine assessment, the patient is found to be increasingly dyspneic and cyanotic, with a rapid decline in his oxygen saturation levels, now reading at 82% despite high-flow nasal cannula support. His respiratory rate has climbed to 32 breaths per minute, accompanied by accessory muscle use and audible wheezing. The patient exhibits signs of increased agitation and confusion, suggesting a worsening of his hypoxemic state. Vital signs reveal a heart rate of 128 beats per minute, blood pressure of 90/55 mmHg, and a low-grade fever of 100.8°F.

The healthcare team swiftly orders repeat arterial blood gases, which indicate a further drop in pH to 7.28, with a PaCO2 of 62 mmHg and PaO2 of 42 mmHg, confirming severe respiratory acidosis and hypoxemia. These alarming values, along with his clinical presentation, point to an acute decompensation of his respiratory function, possibly due to the right-sided pleural effusion or an evolving infectious process. In response, the team initiates non-invasive ventilation to augment his respiratory efforts and improve gas exchange. Concurrently, a decision is made to perform a therapeutic thoracentesis to relieve the pleural effusion and assess for any infectious component.

As the patient is stabilized, attention shifts to the potential for new complications. The persistent hypokalemia, uncorrected despite previous interventions, raises concerns about exacerbating the patient's cardiac arrhythmias. The team considers potassium replacement therapy, balancing it against the risk of further electrolyte disturbances due to ongoing diuretic use. Additionally, the possibility of sepsis is explored, given his fever and declining condition, prompting empiric initiation of broad-spectrum antibiotics while awaiting culture results. This critical juncture in the patient's journey demands advanced clinical reasoning to prioritize interventions and minimize the risk of further deterioration.

Section 3

The healthcare team closely monitors the patient following the initiation of non-invasive ventilation and therapeutic thoracentesis. Within hours, there is a notable improvement in his respiratory effort and oxygenation, with oxygen saturation levels rising to 92%. However, the patient's blood pressure remains precariously low at 88/52 mmHg, despite fluid resuscitation efforts, raising alarms about potential septic shock. The laboratory results from the thoracentesis return, revealing a cloudy, yellowish fluid with a high white cell count and elevated lactate dehydrogenase levels, consistent with an exudative effusion possibly secondary to infection.

Simultaneously, blood cultures drawn earlier reveal the presence of Gram-positive cocci, supporting the hypothesis of a bacterial infection. With the identification of a likely infectious source, the team adjusts the antibiotic regimen to target the specific organism, while continuing broad-spectrum coverage to safeguard against other potential pathogens. Despite these interventions, the patient's renal function begins to decline, evidenced by rising creatinine levels, now at 2.1 mg/dL, and a drop in urine output to less than 20 mL/hour, suggesting the onset of acute kidney injury potentially linked to both sepsis and the effects of diuretics.

Amidst these developments, the team faces critical decisions regarding fluid management, balancing the need for adequate perfusion against the risk of worsening respiratory status due to fluid overload. Furthermore, there is concern about the potential for electrolyte imbalances, particularly with the ongoing hypokalemia and the risk of arrhythmias. This complex interplay of factors requires astute clinical judgment to navigate the patient's fragile state, ensuring that each intervention is carefully weighed to prevent further complications and promote recovery. As the team strategizes the next steps, they must remain vigilant for signs of multi-organ dysfunction and adjust their approach based on the evolving clinical picture.

Section 4

As the healthcare team continues to monitor the patient closely, a new complication emerges. Overnight, the patient begins to exhibit signs of neurological changes, including confusion and agitation, which are new and concerning developments. A rapid neurological assessment reveals that the patient is disoriented to time and place, with a Glasgow Coma Scale (GCS) score dropping to 13 from a previous 15. In light of these changes, an urgent CT scan of the head is ordered to rule out any acute intracranial pathology. Concurrently, further laboratory tests are conducted to assess for potential metabolic causes such as electrolyte disturbances or hypoxia contributing to the altered mental status.

The CT scan returns without evidence of acute intracranial hemorrhage or ischemic stroke, shifting the focus back to possible metabolic derangements. The laboratory results reveal a critically low potassium level of 2.8 mEq/L, alongside a serum sodium level of 131 mEq/L, suggesting ongoing electrolyte imbalances as a likely contributor. These findings prompt the team to initiate a cautious potassium replacement protocol, while being mindful of the patient's cardiac status and the risk of arrhythmias.

With the confirmation of electrolyte disturbances as a potential cause of the altered mental status, the team must strategize an effective management plan. The goal is to correct the imbalances while avoiding rapid shifts that could precipitate further complications. As part of this plan, continuous cardiac monitoring is implemented to detect any arrhythmias, and close attention is paid to the patient's fluid status to prevent exacerbation of the acute kidney injury. The team also considers consulting a nephrologist for expert guidance on managing the delicate balance of fluid and electrolyte replacement in the context of the patient's complex clinical picture. As the team navigates these challenges, they remain vigilant for any signs of further multi-organ dysfunction, ready to adapt their approach as the patient's condition evolves.

Section 5

The healthcare team diligently implements the potassium replacement protocol, administering the electrolyte intravenously at a controlled rate to avoid rapid shifts that could destabilize the patient's cardiac rhythm. Continuous cardiac monitoring is maintained, revealing occasional premature ventricular contractions (PVCs), a concerning sign that underscores the precarious balance the team must maintain. The patient's vital signs show a heart rate of 96 beats per minute, blood pressure of 118/76 mmHg, respiratory rate of 22 breaths per minute, and oxygen saturation fluctuating between 92-94% on 2 liters of oxygen via nasal cannula. These parameters reflect a cardiovascular system under stress, necessitating close observation.

During the course of the intervention, the patient begins to exhibit mild, yet noteworthy, improvements in neurological status. The confusion and agitation show slight amelioration, with the patient now oriented to person but still disoriented to time and place. The Glasgow Coma Scale (GCS) score inches upwards to 14, indicating a positive, albeit cautious, response to the electrolyte correction. However, the team remains vigilant as the patient's fluid status becomes a critical focus. Despite careful monitoring, the patient develops mild peripheral edema, prompting concerns about fluid overload, particularly in the context of the existing acute kidney injury.

Recognizing the delicate interplay between fluid management and electrolyte correction, the team convenes a multidisciplinary meeting, including a nephrologist, to reassess and adjust the treatment plan. The nephrologist suggests a tailored diuretic regimen to address the fluid retention while continuing to correct the electrolyte imbalances judiciously. This collaborative approach aims to stabilize the patient's condition further, knowing that the risk of additional complications, such as heart failure or worsening renal function, remains ever-present. As the team navigates these complexities, they prepare for the possibility of further interventions, including potential dialysis, should the patient's renal function fail to improve.