A patient with heart failure is experiencing acute decompensation, marked by worsening shortness of breath, bilateral crackles, and frothy sputum. The patient is currently on intravenous furosemide therapy. Which nursing intervention is most critical to prioritize for this patient?

B) Monitor the patient's electrolyte levels and report significant changes.

A) Encourage the patient to increase fluid intake to prevent dehydration.

B) Monitor the patient's electrolyte levels and report significant changes.

C) Advise the patient to perform deep breathing exercises to improve oxygenation.

D) Position the patient in a supine position to promote venous return.

A patient with worsening heart failure is exhibiting signs of acute decompensated heart failure, including shortness of breath, bilateral crackles, and frothy sputum. The healthcare team decides to increase the dose of intravenous furosemide. What is the primary nursing consideration when administering this increased diuretic dose?

A) Monitor the patient's blood pressure closely to prevent hypotension.

B) Increase the patient's fluid intake to prevent dehydration.

C) Encourage the patient to ambulate frequently to improve circulation.

D) Monitor the patient's glucose levels to prevent hyperglycemia.

A patient with systolic heart failure is experiencing diuresis with intravenous furosemide, but still has nocturia and pulmonary edema. The patient's ejection fraction is 35% and sodium levels have decreased to 128 mmol/L. What is the most appropriate nursing action to address the patient's condition while preventing further electrolyte imbalance?

B) Administer spironolactone to address fluid overload and manage potassium levels.

A) Increase the dose of intravenous furosemide to enhance fluid removal.

B) Administer spironolactone to address fluid overload and manage potassium levels.

C) Restrict fluid intake to limit further fluid overload.

D) Initiate a low-sodium diet to manage hypertension and fluid retention.

A patient with systolic heart failure and a reduced ejection fraction of 35% is being treated with an increased dose of intravenous furosemide, which has resulted in effective diuresis. However, the patient continues to experience persistent pulmonary edema and hyponatremia. Which of the following interventions should the nurse anticipate in the management plan to address both fluid overload and electrolyte imbalances?

C) Add a potassium-sparing diuretic such as spironolactone.

A) Increase the dose of furosemide to enhance diuresis.

B) Initiate an ACE inhibitor to improve cardiac output and manage hypertension.

C) Add a potassium-sparing diuretic such as spironolactone.

D) Administer hypertonic saline to correct hyponatremia.

A patient with a history of heart failure is being treated with intravenous furosemide for fluid overload. The clinical team decides to adjust the diuretic therapy due to signs of volume depletion. Which of the following assessments should the nurse prioritize to ensure the patient's safety during these medication adjustments?

A) Monitor the patient's blood pressure and heart rate closely for signs of orthostatic changes.

B) Assess the patient's respiratory rate and oxygen saturation for signs of respiratory distress.

C) Evaluate the patient's weight daily to monitor for signs of fluid retention.

D) Observe the patient for signs of increased urination as an indicator of effective diuresis.

A patient receiving diuretic therapy for heart failure is experiencing orthostatic hypotension and compensatory tachycardia. The clinical team has adjusted the treatment plan by reducing intravenous furosemide, adding oral spironolactone, and starting a low-dose ACE inhibitor. What is the primary nursing intervention to prioritize after these changes?

C) Evaluate the patient's blood pressure and heart rate in different positions.

A) Monitor the patient's weight daily and assess for signs of fluid overload.

B) Educate the patient on the importance of increasing fluid intake to prevent dehydration.

C) Evaluate the patient's blood pressure and heart rate in different positions.

D) Encourage the patient to consume a high-potassium diet to counteract diuretic effects.

A patient with heart failure is found to have a potassium level of 3.0 mmol/L and sodium level of 130 mmol/L. The treatment plan includes increasing the dose of spironolactone and starting a potassium supplement. Which of the following is the most important nursing intervention to prevent complications associated with these laboratory findings?

C) Assess the patient for signs of hyperkalemia after initiating potassium supplementation.

A) Monitor the patient's blood pressure for signs of hypotension.

B) Educate the patient on increasing potassium-rich foods in their diet.

C) Assess the patient for signs of hyperkalemia after initiating potassium supplementation.

D) Encourage the patient to drink fluids liberally to correct hyponatremia.

A patient with heart failure is being treated with spironolactone, and recent lab results show a potassium level of 3.0 mmol/L and sodium level of 130 mmol/L. The patient's creatinine has increased to 1.5 mg/dL. Which nursing intervention is the most appropriate to address the electrolyte imbalances while considering the patient's renal function?

A) Increase spironolactone dose and start potassium supplements.

B) Restrict sodium intake and discontinue spironolactone.

C) Start sodium supplements and maintain the current spironolactone dose.

D) Increase fluid intake and discontinue potassium supplements.

A patient with a history of heart failure is experiencing increased dyspnea, mild peripheral edema, and bilateral crackles at the lung bases. Laboratory results reveal hyponatremia with sodium levels at 128 mmol/L. Which nursing intervention is most appropriate to address the current condition while minimizing potential complications?

C) Implement fluid restriction and monitor for electrolyte imbalance

A) Increase fluid intake to correct hyponatremia

B) Administer a higher dose of loop diuretics immediately

C) Implement fluid restriction and monitor for electrolyte imbalance

D) Encourage high-sodium diet to improve sodium levels

A patient with heart failure is experiencing increased dyspnea, peripheral edema, and has a sodium level of 128 mmol/L. The clinical team has adjusted diuretic therapy and implemented fluid restrictions. Which nursing intervention is most appropriate to monitor the effectiveness of the treatment plan?

A) Monitor daily weights and record any changes.

B) Increase fluid intake to promote renal perfusion.

C) Encourage the patient to perform deep breathing exercises.

D) Administer supplementary oxygen to maintain saturation levels above 95%.

Heart failure - Nursing Case Study

Pathophysiology

• Primary mechanism: Decreased cardiac output due to impaired ventricular function leads to insufficient blood supply to meet the body's needs, causing fatigue and organ dysfunction. This often results from conditions like ischemic heart disease or chronic hypertension, which reduce myocardial contractility or increase afterload.

• Secondary mechanism: Neurohormonal activation involving the renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system exacerbates heart failure. Increased angiotensin II and aldosterone result in fluid retention and vasoconstriction, further burdening the heart and worsening symptoms like edema and dyspnea.

• Key complication: Fluid overload from renal sodium retention and increased venous pressures leads to pulmonary congestion and peripheral edema, complicating patient management and increasing hospitalization risk.

Patient Profile

Demographics:

65-year-old male, retired construction worker

History:

• Key past medical history: Hypertension, Type 2 Diabetes, Coronary Artery Disease

• Current medications: Lisinopril, Metformin, Aspirin, Metoprolol, Furosemide

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Increasing shortness of breath and fatigue

• Key symptoms: Swelling in the legs, persistent cough, difficulty breathing while lying flat, weight gain

• Vital signs: Blood pressure 150/95 mmHg, Heart rate 110 bpm, Respiratory rate 24 breaths/min, Oxygen saturation 90% on room air, Temperature 98.6°F

Section 1

Change in Patient Status:

Over the next 24 hours, the patient exhibits a noticeable change in status. His shortness of breath worsens, particularly during minimal exertion, such as walking to the bathroom. He now requires supplemental oxygen to maintain an oxygen saturation above 90%, and his respiratory rate has increased to 28 breaths per minute. The patient is visibly anxious and struggles to complete full sentences due to dyspnea. Additionally, auscultation of the lungs reveals bilateral crackles, suggesting worsening pulmonary congestion. His blood pressure remains elevated at 155/98 mmHg, and his heart rate has increased to 120 bpm.

Further complications arise as the patient reports a new onset of nocturia and a persistent, productive cough with frothy sputum. These symptoms, combined with the escalation in respiratory distress, suggest that the heart failure may be progressing to acute decompensated heart failure. Laboratory results show an elevated BNP (B-type Natriuretic Peptide) level of 950 pg/mL, indicating significant cardiac stress. Serum electrolytes reveal mild hyponatremia with a sodium level of 130 mmol/L, likely due to the effects of diuretic therapy and fluid overload.

The clinical team is prompted to reassess the current management plan, considering the need for more aggressive diuresis and potential adjustments to the patient's medication regimen. A decision is made to increase the dose of intravenous furosemide to address the fluid overload more effectively. The patient is also placed on a low-sodium diet to help manage fluid retention. These adjustments aim to alleviate symptoms and stabilize the patient, while ongoing monitoring will determine the next steps in treatment, including potential consideration for advanced heart failure therapies.

Section 2

As the clinical team implements the new management plan, the initial response to the increased dose of intravenous furosemide is promising. Over the next several hours, the patient begins to diurese effectively, with urine output increasing significantly. The patient reports a slight decrease in dyspnea and finds it somewhat easier to speak in full sentences. Despite these improvements, the patient continues to experience nocturia and a persistent cough, although the sputum appears less frothy. Vital signs indicate a slight improvement, with a decrease in respiratory rate to 24 breaths per minute and a heart rate that stabilizes at 110 bpm. However, blood pressure remains elevated at 150/95 mmHg, necessitating ongoing monitoring and potential antihypertensive adjustments.

New diagnostic results add another layer to the clinical picture. A follow-up chest X-ray reveals persistent pulmonary edema, suggesting that while diuresis is effective, the fluid overload is yet to be fully controlled. Echocardiography is conducted to reassess cardiac function and reveals a reduced ejection fraction of 35%, consistent with systolic heart failure and explaining the patient's ongoing symptoms. The lab work shows a further decline in sodium levels to 128 mmol/L, raising concerns about the balance between effective diuresis and the maintenance of electrolyte stability.

In light of these findings, the clinical team recognizes the need to refine the therapeutic approach further. Consideration is given to introducing an ACE inhibitor to help improve cardiac output and control hypertension. The team also discusses the potential need for additional diuretic classes, such as spironolactone, to manage the fluid overload while minimizing electrolyte disturbances. As the patient's condition remains tenuous, careful titration of medications and close monitoring of electrolytes and renal function become paramount. This strategic adjustment aims to optimize heart failure management and prevent the development of further complications, setting the stage for the next phase of the patient's recovery process.

Section 3

As the clinical team continues to monitor the patient closely, a change in the patient's status becomes apparent. Despite the initial improvement with increased diuresis, the patient begins to exhibit signs of volume depletion. The patient reports feeling increasingly fatigued and lightheaded when attempting to sit up or move. On examination, orthostatic hypotension is noted, with blood pressure dropping to 110/70 mmHg upon standing. Heart rate increases to 120 bpm, suggesting compensatory tachycardia. These findings indicate that while fluid overload remains a concern, the aggressive diuresis may now be contributing to intravascular volume depletion.

In response to these developments, the clinical team reviews the current medication regimen. The decision is made to adjust the diuretic therapy by reducing the dose of intravenous furosemide and introducing oral spironolactone to balance potassium levels and provide a more gradual diuretic effect. The team also cautiously initiates an ACE inhibitor, starting with a low dose to assess tolerance, with the aim of improving cardiac output and further reducing afterload. Laboratory tests are prioritized to monitor sodium, potassium, and renal function, as electrolyte imbalances and renal impairment are potential complications of the revised treatment plan.

As these therapeutic adjustments are implemented, the patient's condition requires continuous evaluation to ensure stability and prevent further complications. The clinical team emphasizes the importance of monitoring for signs of electrolyte imbalance or renal dysfunction. They also educate the patient on recognizing symptoms of hypotension or electrolyte disturbances. This proactive approach aims to carefully navigate the balance between effective fluid management and maintaining hemodynamic stability, setting the foundation for the patient's ongoing recovery and transition to a more stable state.

Section 4

As the revised treatment plan is implemented, the clinical team remains vigilant in monitoring the patient's response. Over the next 48 hours, the patient begins to exhibit signs of electrolyte imbalance, a potential complication that was anticipated. Laboratory results reveal a potassium level of 3.0 mmol/L, indicating hypokalemia despite the introduction of spironolactone. Sodium levels have decreased to 130 mmol/L, suggesting hyponatremia. Renal function tests show a slight increase in creatinine to 1.5 mg/dL from a baseline of 1.2 mg/dL, necessitating careful monitoring for potential renal impairment.

In response to these findings, the clinical team takes decisive action to address the electrolyte disturbances. The spironolactone dose is increased, and the patient is started on a potassium supplement to correct the hypokalemia. Sodium intake is adjusted to address the hyponatremia, with close monitoring of fluid balance to avoid exacerbating the heart failure. The ACE inhibitor dose is maintained at a low level to continue providing afterload reduction benefits while minimizing the risk of further renal compromise.

As these interventions are carried out, the patient's condition stabilizes. The orthostatic hypotension improves, with blood pressure readings showing less variability between lying and standing positions. Fatigue and lightheadedness lessen, indicating a positive response to the adjusted treatment plan. The clinical team continues to educate the patient on the importance of adhering to the medication regimen and recognizing symptoms that warrant immediate medical attention. Through these proactive measures, the patient is gradually steered towards a more stable state, setting the stage for further rehabilitation and management of heart failure.

Section 5

As the patient's condition stabilizes, the clinical team remains vigilant for any new complications. Over the next 24 hours, the patient begins to experience increased dyspnea and mild peripheral edema, raising concerns about fluid overload despite adjustments in the treatment regimen. Vital signs reveal a heart rate of 92 bpm, blood pressure of 138/82 mmHg, respiratory rate of 24 breaths per minute, and oxygen saturation of 91% on room air. Auscultation of the lungs indicates bilateral crackles at the bases, suggesting pulmonary congestion. These findings, coupled with the newly developed edema, prompt the team to reassess the patient's fluid status and diuretic therapy.

Laboratory results return with a further decline in sodium levels to 128 mmol/L, while potassium levels have improved to 3.5 mmol/L. Renal function remains stable with creatinine at 1.5 mg/dL. Given the persistent hyponatremia and signs of fluid overload, the clinical team decides to cautiously adjust diuretic therapy while implementing a more stringent fluid restriction protocol. Loop diuretics are reintroduced at a low dose to alleviate pulmonary congestion while minimizing the risk of exacerbating electrolyte imbalances or renal function. The patient is closely monitored for any signs of dehydration or worsening renal impairment.

With these adjustments, the clinical team continues to engage in patient education, emphasizing the importance of adhering to fluid restrictions and dietary modifications. Efforts are made to ensure the patient understands the signs and symptoms of worsening heart failure, such as increased shortness of breath or significant weight gain, which would necessitate immediate medical attention. By addressing these complications promptly and adjusting the treatment plan accordingly, the clinical team aims to create a more stable environment for the patient, paving the way for ongoing management and eventual discharge planning.