A patient with a history of heart failure and recent myocardial injury presents with dyspnea, bilateral crackles, and pitting edema. The medical team initiates oxygen therapy, nitroglycerin, and intravenous furosemide. Which of the following nursing assessments is most critical to perform to evaluate the effectiveness of these interventions?

B) Assessing for reduction in crackles and dyspnea

A) Monitoring blood pressure and heart rate

B) Assessing for reduction in crackles and dyspnea

C) Checking the patient's weight daily

D) Evaluating the patient's skin turgor and mucous membranes

A nurse is caring for a patient with acute coronary syndrome and heart failure exacerbation who is receiving treatment with nitroglycerin and furosemide. Which assessment finding would indicate that the patient's condition is worsening and requires immediate intervention?

C) Development of new-onset confusion

D) Reduction in chest pain with exertion

A patient with acute decompensated heart failure and possible acute coronary syndrome is showing signs of respiratory distress and hypotension. Considering the current treatment plan, which nursing intervention is most critical to prioritize at this time?

A) Initiate high-flow nasal cannula oxygen therapy to improve oxygenation

B) Administer a vasopressor to support blood pressure

C) Increase the dose of furosemide to reduce pulmonary congestion

D) Prepare the patient for urgent coronary angiography

A patient with acute decompensated heart failure and suspected acute coronary syndrome is exhibiting increased respiratory distress and signs of shock. The healthcare team is considering several interventions, including adjusting oxygen therapy, administering diuretics, and initiating a vasopressor. Which of the following nursing assessments is most critical to prioritize in this situation to guide immediate treatment decisions?

A) Monitoring blood pressure and heart rate closely for changes after vasopressor initiation.

B) Checking urine output to assess the effectiveness of increased furosemide dose.

C) Evaluating skin color and temperature for signs of peripheral perfusion.

D) Assessing mental status for any changes indicating worsening hypoxia or cerebral perfusion.

A patient with known ischemic heart disease is undergoing treatment for acute decompensated heart failure. Following the initiation of high-flow nasal cannula oxygen and furosemide, the patient shows improvements in oxygen saturation and urine output, but a sudden drop in urine output to less than 20 mL per hour is noted. The nurse should prioritize which intervention to address this change?

B) Reassess fluid status and consider reducing diuretic therapy.

A) Increase the dose of furosemide to enhance diuresis.

B) Reassess fluid status and consider reducing diuretic therapy.

C) Administer an additional bolus of intravenous fluids to improve renal perfusion.

D) Prepare for immediate dialysis to address potential renal failure.

A patient with acute decompensated heart failure shows initial improvement in oxygenation and diuresis but then experiences a significant drop in urine output to less than 20 mL per hour. What is the nurse's priority action to address this change in the patient's condition?

B) Assess the patient's fluid status and consider reducing diuretics.

A) Increase the dose of furosemide to enhance diuresis.

B) Assess the patient's fluid status and consider reducing diuretics.

C) Immediately increase the vasopressor infusion rate.

D) Prepare the patient for emergency dialysis.

A patient in the ICU has recently undergone percutaneous coronary intervention (PCI) for critical stenosis in the left anterior descending artery. Despite improvement in hemodynamic status, the patient exhibits low urine output and rising serum creatinine levels, indicative of acute kidney injury (AKI). Which nursing intervention should be prioritized to address the patient's renal function while maintaining cardiovascular stability?

C) Implement advanced hemodynamic monitoring to guide fluid management decisions.

A) Administer a diuretic to increase urine output and decrease fluid overload.

B) Increase intravenous fluid administration to enhance renal perfusion.

C) Implement advanced hemodynamic monitoring to guide fluid management decisions.

D) Withhold all fluids and medications until renal function stabilizes.

A patient has undergone percutaneous coronary intervention (PCI) for critical stenosis in the left anterior descending artery. Post-procedure, the patient's urine output is less than 15 mL per hour, and serum creatinine levels have risen, indicating potential acute kidney injury. Which nursing intervention is most appropriate to address the patient's current renal status while maintaining cardiovascular stability?

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

A) Increase the rate of intravenous fluids to improve renal perfusion.

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

C) Adjust the patient's position to improve renal blood flow.

D) Initiate continuous renal replacement therapy (CRRT) immediately.

A patient 24 hours post-PCI is showing signs of respiratory distress with increased work of breathing, crackles on auscultation, and oxygen saturation of 90% on room air. The chest X-ray indicates fluid overload with diffuse interstitial markings and pleural effusions. What is the most appropriate nursing intervention to address the patient's respiratory distress while considering their renal status?

C) Initiate oxygen therapy and consult the physician about starting a low-dose diuretic.

A) Administer a high-dose loop diuretic immediately to reduce fluid overload.

B) Increase the rate of intravenous fluids to improve renal perfusion.

C) Initiate oxygen therapy and consult the physician about starting a low-dose diuretic.

D) Encourage the patient to sit up and perform deep breathing exercises to improve oxygenation.

A patient is 24 hours post-percutaneous coronary intervention (PCI) and presents with increased work of breathing, bilateral crackles, and a drop in oxygen saturation. A chest X-ray shows diffuse interstitial markings and mild bilateral pleural effusions. Given these findings, which of the following nursing actions is the most appropriate to address the patient's condition?

B) Administer a low-dose diuretic as prescribed and monitor urine output

A) Increase the rate of intravenous fluids to enhance renal perfusion

B) Administer a low-dose diuretic as prescribed and monitor urine output

C) Encourage deep breathing exercises to improve oxygenation

D) Place the patient in a supine position to facilitate lung expansion

Cardiac - Nursing Case Study

Pathophysiology

• Primary mechanism: Decreased cardiac output occurs when the heart's ability to pump blood is impaired, often due to myocardial damage or valve dysfunction, leading to insufficient blood supply to meet the body's demands.

• Secondary mechanism: Compensatory mechanisms, such as activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS), initially support blood pressure and perfusion but eventually contribute to heart failure progression by increasing cardiac workload and fluid retention.

• Key complication: The resulting fluid overload can lead to pulmonary congestion and peripheral edema, exacerbating symptoms and reducing quality of life, necessitating careful monitoring and management in clinical settings.

Patient Profile

Demographics:

55-year-old male, construction worker

History:

• Key past medical history: Hypertension, Type 2 Diabetes, Hyperlipidemia

• Current medications: Lisinopril, Metformin, Atorvastatin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Chest pain and shortness of breath

• Key symptoms: Fatigue, dizziness, occasional palpitations

• Vital signs: Blood pressure 145/95 mmHg, heart rate 110 bpm, respiratory rate 22 breaths per minute, temperature 98.6°F, oxygen saturation 93% on room air

Section 1

As the clinical team conducts an initial assessment of the patient, several concerning findings emerge. The patient is diaphoretic and appears anxious, with visible difficulty in breathing. Lung auscultation reveals bilateral crackles in the lower lobes, suggesting pulmonary congestion. Examination of the extremities shows mild pitting edema in the ankles, indicative of fluid overload. A 12-lead ECG is performed, revealing sinus tachycardia with non-specific ST segment changes, raising concerns about possible ischemic changes or underlying myocardial dysfunction. The patient reports that the chest pain radiates to his left shoulder and worsens with exertion, aligning with patterns of angina.

Laboratory results return, further complicating the clinical picture. The patient's troponin levels are mildly elevated, suggesting myocardial injury, while BNP levels are significantly elevated, indicating heart failure exacerbation. Renal function tests show a slight increase in creatinine, hinting at renal impairment likely due to decreased perfusion or as a side effect of RAAS activation. These results prompt the healthcare team to consider acute coronary syndrome alongside heart failure exacerbation.

In response to these findings, the medical team initiates treatment focused on stabilizing the patient's cardiovascular status. Oxygen therapy is started to improve oxygen saturation, and the patient is given nitroglycerin to relieve chest pain and reduce cardiac workload. Furosemide is administered intravenously to address fluid overload and improve respiratory function. As these interventions are underway, continuous monitoring of the patient's hemodynamic status and renal function is crucial, as the risk of further complications remains high. The team plans for further cardiac imaging to assess the extent of myocardial damage and considers adjustments to the patient's medication regimen to optimize heart failure management and mitigate future risks. These steps lay the groundwork for the next phase of the patient's care journey.

Section 2

As the medical team continues to monitor the patient, a change in status becomes apparent. Despite initial interventions, the patient’s condition shows signs of deterioration. His respiratory rate increases to 28 breaths per minute, and oxygen saturation drops to 88% on room air, necessitating an escalation in oxygen therapy. The patient becomes increasingly tachypneic, with accessory muscle use indicating worsening respiratory distress. The crackles in both lung fields have progressed to wheezing, suggesting bronchospasm or further fluid accumulation. Heart rate remains elevated at 110 beats per minute, and blood pressure has decreased to 98/62 mmHg, raising concerns of possible cardiogenic shock.

New laboratory results arrive, indicating a further rise in troponin levels, confirming ongoing myocardial injury. The BNP level remains elevated, consistent with acute heart failure exacerbation, while the creatinine level has increased to 2.1 mg/dL, indicating worsening renal function. A repeat ECG now shows more pronounced ST segment depression, consistent with ischemia. These findings prompt the team to reassess the management plan urgently, considering the possibility of acute decompensated heart failure with underlying acute coronary syndrome.

In response, the clinical team decides to intensify treatment efforts. High-flow nasal cannula oxygen is initiated to improve oxygenation. The dose of furosemide is increased to enhance diuresis and reduce pulmonary congestion. A vasopressor is considered to support blood pressure and improve perfusion, as the risk of multi-organ dysfunction looms. Additionally, the plan includes urgent coronary angiography to identify and address any significant coronary artery blockages. These measures are critical to stabilizing the patient's condition and mitigating the risk of further complications in his cardiac and renal systems. The healthcare team remains vigilant, aware that this pivotal phase will determine the trajectory of the patient's recovery.

Section 3

As the clinical team implements the intensified treatment plan, the patient's response to interventions is carefully monitored. Within the first hour of starting high-flow nasal cannula oxygen, the patient's oxygen saturation begins to improve, rising steadily to 92%. This improvement in oxygenation brings a slight decrease in respiratory rate to 24 breaths per minute, though accessory muscle use persists, indicating ongoing respiratory effort. The increased dose of furosemide leads to a noticeable diuresis, with urine output increasing to approximately 100 mL per hour, suggesting a positive response in reducing pulmonary congestion.

Despite these initial encouraging signs, the patient's hemodynamic status continues to be precarious. The heart rate has decreased slightly to 105 beats per minute, but blood pressure remains low at 94/60 mmHg, prompting the team to initiate a low-dose vasopressor infusion to support cardiac output and maintain vital organ perfusion. The decision to proceed with coronary angiography is confirmed, given the persistent ST segment depression on ECG and elevated troponin levels, which signal ongoing ischemic injury.

During this critical phase, the team remains alert to potential complications. A new concern arises with a sudden drop in urine output, now less than 20 mL per hour, raising alarms about worsening renal function and possible acute kidney injury. This change necessitates further evaluation of fluid status and renal perfusion, as the balance between diuresis and maintaining adequate blood pressure becomes increasingly delicate. The healthcare team prepares to adapt the management strategy based on the coronary angiography results, which will provide a clearer picture of the underlying cardiac pathology, guiding further therapeutic interventions and shaping the next steps in the patient's recovery journey.

Section 4

As the clinical team continues to monitor the patient closely, the coronary angiography reveals significant findings that reshape the treatment approach. The procedure identifies a critical stenosis in the left anterior descending artery, while also noting moderate disease in the right coronary artery. These findings confirm the suspicion of ongoing myocardial ischemia, which correlates with the persistent ST segment depression and elevated troponin levels. The decision is made to proceed with percutaneous coronary intervention (PCI) to address the critical lesion and restore adequate blood flow to the myocardium.

Following the PCI, the patient's hemodynamic status shows tentative signs of stabilization. The blood pressure edges up slightly to 98/65 mmHg, and heart rate stabilizes around 100 beats per minute, suggesting some improvement in cardiac output. However, despite these encouraging signs, the patient's urine output remains concerningly low, at less than 15 mL per hour, indicating potential acute kidney injury. Serum creatinine levels have risen from a baseline of 1.0 mg/dL to 2.2 mg/dL, confirming the suspicion of deteriorating renal function.

The clinical team is now faced with the complex task of balancing fluid management and renal perfusion while ensuring cardiovascular stability. Discussions revolve around adjusting diuretic therapy and considering renal protective strategies, such as the cautious use of intravenous fluids and potential nephroprotective agents. The team also explores the use of advanced hemodynamic monitoring to guide further interventions, aiming to optimize the patient's recovery while mitigating the risk of further renal compromise. As the patient remains in a critical phase of treatment, these decisions will play a pivotal role in determining the next steps of the care plan.

Section 5

As the clinical team continues to navigate the delicate balance of treatment, a new complication emerges that demands immediate attention. Within 24 hours post-PCI, the patient begins to exhibit signs of respiratory distress, including increased work of breathing and a respiratory rate climbing to 28 breaths per minute. Auscultation reveals bilateral crackles, particularly in the lower lung fields, suggestive of pulmonary congestion. Concurrently, the oxygen saturation drops to 90% on room air, necessitating supplemental oxygen to maintain adequate levels.

In light of these developments, a chest X-ray is promptly ordered, revealing diffuse interstitial markings and mild bilateral pleural effusions, consistent with fluid overload. This worsening respiratory status, coupled with the low urine output, indicates that the patient's fluid balance is tipping towards overload, complicating the clinical picture. The team must now reassess the fluid management strategy, particularly the cautious administration of intravenous fluids, while considering the introduction of diuretics to mitigate pulmonary congestion without exacerbating the renal impairment.

The clinical team convenes to weigh the potential risks and benefits of adjusting the current treatment plan. They deliberate on the judicious use of a low-dose diuretic, aiming to relieve pulmonary symptoms while closely monitoring renal function and hemodynamic parameters. This scenario underscores the need for vigilant monitoring and rapid response to the evolving clinical situation, as the team strives to stabilize the patient's condition and prevent further complications. The decisions made in this critical phase will significantly influence the patient's trajectory and recovery.