A patient with an anterior wall myocardial infarction is experiencing new-onset hypotension and signs of pulmonary edema. Which intervention should the nurse prioritize to address the patient's deteriorating condition?

C) Initiate inotropic support to enhance cardiac contractility.

A) Increase the rate of intravenous fluids to improve blood pressure.

B) Administer a dose of furosemide to reduce pulmonary congestion.

C) Initiate inotropic support to enhance cardiac contractility.

D) Prepare the patient for immediate percutaneous coronary intervention (PCI).

A patient experiencing an anterior wall myocardial infarction is showing signs of cardiogenic shock with hypotension and pulmonary edema. In addition to administering supplemental oxygen, what is the priority nursing intervention to improve the patient's hemodynamic status?

B) Administer inotropic agents to improve cardiac contractility.

A) Initiate a fluid bolus to increase blood pressure.

B) Administer inotropic agents to improve cardiac contractility.

C) Increase the dosage of nitroglycerin to reduce chest pain.

D) Place the patient in Trendelenburg position to enhance venous return.

A nurse is caring for a patient with cardiogenic shock secondary to acute myocardial infarction, who is currently receiving dobutamine infusion. Which of the following assessments is most critical for the nurse to perform to evaluate the effectiveness of the inotropic therapy?

B) Assess for improvement in urinary output.

A) Monitor for changes in heart rate and rhythm.

B) Assess for improvement in urinary output.

C) Observe for reduction in respiratory rate.

D) Evaluate for changes in mental status.

A nurse is caring for a patient experiencing cardiogenic shock due to an acute myocardial infarction. Which of the following interventions should the nurse prioritize to improve systemic perfusion and prevent further organ dysfunction?

C) Initiating inotropic support with dobutamine as prescribed and monitoring hemodynamic response

A) Administering intravenous fluids rapidly to increase blood volume

B) Positioning the patient in a Trendelenburg position to enhance venous return

C) Initiating inotropic support with dobutamine as prescribed and monitoring hemodynamic response

D) Preparing the patient for immediate dialysis to address renal hypoperfusion

A patient receiving dobutamine for inotropic support has shown modest hemodynamic improvement but remains tachypneic with signs of inadequate perfusion. An angiogram reveals critical stenosis of the left anterior descending artery, necessitating urgent PCI. The patient's serum creatinine has risen to 2.5 mg/dL, indicating potential acute kidney injury. Which nursing intervention is most appropriate to optimize renal perfusion while preparing for PCI?

C) Cautiously administer intravenous fluids to maintain adequate renal perfusion without causing fluid overload.

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

B) Administer a diuretic to prevent fluid overload and protect renal function.

C) Cautiously administer intravenous fluids to maintain adequate renal perfusion without causing fluid overload.

D) Delay PCI until renal function stabilizes to avoid further renal compromise.

A patient with cardiogenic shock is being prepared for percutaneous coronary intervention (PCI) due to critical stenosis of the left anterior descending artery. The patient is also at risk for acute kidney injury as indicated by a rising serum creatinine level. What is the most appropriate nursing intervention to help prevent further renal damage while balancing cardiac function?

C) Monitor urine output and adjust fluid therapy accordingly.

A) Administer diuretics to reduce fluid overload.

B) Increase intravenous fluid rate to improve renal perfusion.

C) Monitor urine output and adjust fluid therapy accordingly.

D) Limit fluid intake to prevent cardiac strain.

A patient who recently underwent percutaneous coronary intervention (PCI) for a blockage in the left anterior descending artery is now showing signs of low cardiac output and decreased tissue perfusion. Which nursing intervention is most appropriate to prioritize at this time to support this patient's hemodynamic status?

B) Prepare the patient for potential insertion of an intra-aortic balloon pump (IABP).

A) Administer intravenous fluids to increase preload.

B) Prepare the patient for potential insertion of an intra-aortic balloon pump (IABP).

C) Increase the oxygen flow rate on the non-rebreather mask to 15 L/min.

D) Position the patient in Trendelenburg to enhance venous return.

A patient has undergone a successful PCI with stent placement but now presents with hypotension, tachycardia, increased respiratory rate, and signs of poor perfusion. Laboratory results show elevated creatinine and lactate levels. Which intervention should the nurse prioritize to stabilize the patient's hemodynamic status and prevent further organ dysfunction?

B) Initiate dobutamine infusion to enhance cardiac output.

A) Administer a fluid bolus to improve blood pressure and perfusion.

B) Initiate dobutamine infusion to enhance cardiac output.

C) Prepare for the insertion of an intra-aortic balloon pump (IABP).

D) Increase oxygen flow rate on the non-rebreather mask to 100%.

A patient with cardiogenic shock and pulmonary edema is being managed with an intra-aortic balloon pump (IABP) and diuretics. Despite these interventions, the patient's condition remains unstable with elevated creatinine and lactate levels. Which of the following nursing interventions is most appropriate to address the patient's current status?

A) Increase the rate of diuretic administration to rapidly reduce fluid overload.

C) Increase the oxygen flow rate to improve oxygen saturation.

D) Adjust the intra-aortic balloon pump (IABP) timing to enhance cardiac output.

A patient with suspected cardiogenic shock displays new onset confusion, jugular venous distension, and crackles upon auscultation. The nursing team is considering the administration of diuretics. What is the primary nursing consideration in this situation?

B) Assess renal function before administering diuretics to prevent worsening renal impairment.

A) Administer diuretics immediately to resolve pulmonary congestion.

B) Assess renal function before administering diuretics to prevent worsening renal impairment.

C) Increase oxygen delivery to improve cerebral perfusion before administering diuretics.

D) Delay diuretics until the patient is hemodynamically stable.

myocardial infarction - Nursing Case Study

Pathophysiology

• Primary mechanism: Coronary artery occlusion due to atherosclerotic plaque rupture leads to thrombosis. This drastically reduces blood flow to a section of the heart muscle, resulting in ischemia and oxygen deprivation.

• Secondary mechanism: Prolonged ischemia triggers myocardial cell death (necrosis) because of inadequate ATP production and accumulation of toxic metabolites, leading to irreversible damage to the heart tissue.

• Key complication: If untreated, myocardial infarction can lead to heart failure, arrhythmias, or cardiogenic shock due to impaired cardiac contractility and electrical stability.

Patient Profile

Demographics:

57-year-old male, construction worker

History:

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

• Current medications: Lisinopril, Metformin, Atorvastatin, Aspirin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Chest pain radiating to the left arm

• Key symptoms: Shortness of breath, sweating, nausea, palpitations

• Vital signs: Blood pressure 150/95 mmHg, heart rate 110 bpm, respiratory rate 24 breaths per minute, temperature 98.6°F, oxygen saturation 92% on room air

Section 1

As the medical team begins their initial assessment, they quickly recognize the classic presentation of an acute myocardial infarction (MI). The patient, still experiencing chest pain and left arm radiation, is placed on supplemental oxygen due to his low oxygen saturation of 92%. A 12-lead electrocardiogram (ECG) reveals ST-segment elevation in the anterior leads, indicating an anterior wall MI. The team initiates a protocol for acute coronary syndrome, which includes administering nitroglycerin for pain relief, and morphine for unrelieved pain, closely monitoring the patient's vital signs and symptom progression.

Further diagnostic results reveal elevated cardiac biomarkers, with troponin levels significantly above the normal range, confirming myocardial injury. The patient's blood glucose level is also critically high at 250 mg/dL, complicating the management of his Type 2 Diabetes and increasing the risk for further ischemic damage. These findings suggest that the infarction is extensive, and there is concern about the extent of myocardial damage and potential complications such as heart failure or arrhythmias.

Despite the interventions, the patient's condition begins to deteriorate. He develops new-onset hypotension, with blood pressure dropping to 85/60 mmHg, and exhibits signs of pulmonary edema, including increased respiratory distress and crackles upon auscultation of the lungs. These changes suggest the development of cardiogenic shock, a moderate complication that requires immediate intervention. The healthcare team must now consider advanced therapies, such as inotropic support and potential revascularization procedures, to stabilize the patient's hemodynamic status and improve cardiac output. This development necessitates further clinical reasoning to prioritize interventions that will address both the acute MI and the emerging complications effectively.

Section 2

As the patient's condition continues to decline, the healthcare team conducts a thorough reassessment to identify the underlying causes of the new symptoms. Vital signs now indicate a heart rate of 120 bpm, respiratory rate of 28 breaths per minute, and persistent hypotension with a blood pressure of 82/55 mmHg. The patient's skin is clammy and cool to the touch, and he remains diaphoretic, signaling worsening perfusion. A repeat ECG shows persistent ST-segment elevation, and new Q waves are emerging in the anterior leads, indicating ongoing myocardial necrosis despite initial interventions.

In response to the declining hemodynamic status, the team orders an urgent echocardiogram, which reveals severely reduced left ventricular ejection fraction at 30%, consistent with significant myocardial dysfunction. Additionally, the presence of moderate mitral regurgitation is noted, likely secondary to papillary muscle dysfunction from ischemic injury. Laboratory tests show worsening renal function, with serum creatinine rising to 2.3 mg/dL, suggesting renal hypoperfusion as a complication of cardiogenic shock.

To address these developments, the medical team initiates inotropic support with dobutamine to enhance cardiac contractility and improve systemic perfusion. Concurrently, discussions are underway to evaluate the patient for urgent coronary angiography and potential percutaneous coronary intervention (PCI) to restore coronary blood flow and limit further myocardial damage. This complex scenario requires careful balancing of interventions to manage the acute myocardial infarction, mitigate cardiogenic shock, and prevent further organ dysfunction, underscoring the need for ongoing reassessment and adaptation of the treatment plan. As the team prepares for potential revascularization, they continue to monitor the patient's response to inotropic therapy and adjust treatment as needed to stabilize his condition.

Section 3

As the medical team closely monitors the patient's response to the initiated inotropic support with dobutamine, they observe a modest improvement in his hemodynamic status. The patient's heart rate stabilizes at 110 bpm, and his blood pressure shows a slight improvement, now reading 90/60 mmHg. Despite these positive changes, the patient remains tachypneic with a respiratory rate of 26 breaths per minute and continues to exhibit signs of inadequate perfusion, as evidenced by his cool, clammy skin and persistent diaphoresis. The team recognizes that while the inotropic therapy is providing some stabilization, it is not sufficient to address the underlying ischemic burden and myocardial dysfunction.

In light of the patient's ongoing compromised status, the decision is made to proceed with urgent coronary angiography. The angiogram reveals a critical stenosis of the left anterior descending artery, confirming the suspicion of a significant culprit lesion. This finding underscores the need for immediate percutaneous coronary intervention (PCI) to restore adequate blood flow to the affected myocardial region. As preparations for the PCI are underway, the healthcare team continues to carefully monitor renal function, noting a serum creatinine level that has risen slightly to 2.5 mg/dL. This indicates persistent renal hypoperfusion and raises concerns about potential acute kidney injury if perfusion is not rapidly optimized.

The team discusses the necessity of balancing fluid management with the risk of exacerbating renal function, choosing to cautiously administer intravenous fluids to support renal perfusion while avoiding fluid overload, which could further strain the already compromised cardiac function. This complex interplay of managing cardiogenic shock, addressing myocardial ischemia, and preventing further renal damage requires vigilant reassessment and a multidisciplinary approach. As the team moves forward with the PCI, they remain acutely aware of the need for dynamic adjustments in the treatment plan to optimize outcomes and mitigate additional complications.

Section 4

As the PCI is successfully completed, restoring patency to the left anterior descending artery with stent placement, the patient's coronary perfusion improves. However, despite this intervention, the clinical team observes that the patient's condition remains precarious. Vital signs indicate a continued struggle; his heart rate is now 105 bpm, but blood pressure remains low at 88/58 mmHg, and his respiratory rate has increased to 28 breaths per minute. The patient's oxygen saturation drops slightly to 91% on 2L nasal cannula, prompting escalation to a non-rebreather mask for supplemental oxygen. His skin remains cool and clammy, and capillary refill is delayed, indicating ongoing peripheral hypoperfusion.

Laboratory results reveal worsening renal function, with serum creatinine rising further to 3.0 mg/dL, signaling acute kidney injury likely due to persistent low cardiac output and possibly exacerbated by contrast-induced nephropathy from the angiography. Additionally, lactate levels have increased to 3.5 mmol/L, suggesting inadequate tissue perfusion and a shift towards anaerobic metabolism. These changes highlight the need for cautious yet proactive management to stabilize his hemodynamics and support organ function.

Given these developments, the healthcare team contemplates the addition of mechanical circulatory support, such as an intra-aortic balloon pump (IABP), to augment cardiac output and improve systemic perfusion. The decision-making process involves weighing the potential benefits against the risks of invasive procedures, especially in light of the patient's compromised renal status. As they deliberate, the team emphasizes the importance of continuous hemodynamic monitoring, frequent reassessment of fluid status, and collaboration with nephrology and cardiology specialists to optimize the patient's care trajectory and prevent further deterioration.

Section 5

As the clinical team continues to monitor the patient's status, they note a concerning change in his condition. Despite the initiation of the intra-aortic balloon pump (IABP) for mechanical circulatory support, his blood pressure remains marginally improved at 92/60 mmHg, and his heart rate has increased further to 115 bpm. The respiratory rate remains elevated at 30 breaths per minute, and oxygen saturation has stabilized slightly at 93% with the non-rebreather mask. However, there is new onset of confusion and restlessness, which raises concerns about cerebral perfusion and potential hypoxemia.

The nursing team performs a comprehensive assessment, revealing jugular venous distension and crackles upon auscultation of the lungs, suggestive of pulmonary congestion. This finding, coupled with the patient's altered mental status, prompts the team to hypothesize that he is developing cardiogenic shock with pulmonary edema. The decision is made to administer diuretics cautiously, balancing the need for reducing fluid overload with the risk of exacerbating his renal impairment.

New laboratory results show further increases in serum creatinine to 3.5 mg/dL and a rise in lactate levels to 4.2 mmol/L, indicating ongoing renal compromise and inadequate perfusion. In light of these developments, the interdisciplinary team, including cardiology and nephrology, discusses the potential for continuous renal replacement therapy (CRRT) to manage fluid balance and support renal function. The team emphasizes the need for vigilant monitoring and adjustments to the therapeutic plan, as they strive to stabilize the patient's condition and prevent further complications in this critical phase of his care.