A patient with an acute inferior wall myocardial infarction is being prepared for emergent PCI. The nurse notes persistent chest pain and a heart rate of 120 bpm with premature ventricular contractions. Which immediate nursing intervention is most appropriate to stabilize the patient before transfer to the catheterization lab?

B) Increase the supplemental oxygen to maintain saturation above 95%.

A) Administer an additional dose of aspirin.

B) Increase the supplemental oxygen to maintain saturation above 95%.

C) Initiate a continuous infusion of beta-blockers to manage the heart rate.

D) Prepare to administer an antiarrhythmic agent to address the PVCs.

A patient with an inferior wall myocardial infarction is experiencing persistent chest pain and premature ventricular contractions despite initial treatment. Which nursing intervention is the highest priority to prevent further cardiac complications?

D) Ensure the patient is prepared for emergent percutaneous coronary intervention.

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

B) Administer a beta-blocker to reduce heart rate and myocardial oxygen demand.

C) Prepare for defibrillation in anticipation of ventricular fibrillation.

D) Ensure the patient is prepared for emergent percutaneous coronary intervention.

A patient who recently underwent coronary stent placement is exhibiting signs of cardiogenic shock with a reduced ejection fraction and respiratory acidosis. Which nursing intervention is most critical to improve the patient's hemodynamic status and prevent further deterioration?

C) Administer a vasopressor infusion to maintain adequate blood pressure and perfusion.

A) Increase the rate of intravenous fluid administration to enhance preload.

B) Initiate a high-flow oxygen therapy to correct hypoxemia and support respiratory function.

C) Administer a vasopressor infusion to maintain adequate blood pressure and perfusion.

D) Encourage the patient to ambulate to improve circulation and oxygenation.

A patient has been diagnosed with inferior wall myocardial infarction and has undergone a successful placement of a drug-eluting stent. Post-procedure, the patient develops cardiogenic shock. Which nursing intervention is the priority to stabilize the patient's hemodynamic status?

A) Administer supplemental oxygen to improve tissue oxygenation.

B) Initiate a fluid bolus to increase preload and improve cardiac output.

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

A patient in the ICU is being treated for myocardial damage and metabolic acidosis, with ongoing signs of respiratory distress and hypokalemia. Which nursing intervention should be prioritized to address the patient's current clinical status and potential complications?

A) Initiate continuous ECG monitoring to assess for arrhythmias.

B) Increase diuretic dose to further reduce pulmonary congestion.

C) Administer supplemental oxygen to improve PaO2 levels.

D) Prepare for potential intubation and mechanical ventilation.

A patient is being monitored for ongoing myocardial damage and respiratory distress. The nursing team notes metabolic acidosis with a pH of 7.35 and hypokalemia. Despite potassium replacement therapy, the patient's condition remains tenuous. Which intervention should the nurse prioritize to address the metabolic acidosis and improve the patient's clinical condition?

B) Increase the rate of oxygen delivery to improve oxygenation.

A) Administer sodium bicarbonate to correct the metabolic acidosis.

B) Increase the rate of oxygen delivery to improve oxygenation.

C) Initiate continuous ECG monitoring to detect arrhythmias.

D) Adjust diuretic therapy to increase renal excretion of acids.

A patient undergoing potassium replacement therapy exhibits new-onset ventricular ectopy, decreased cardiac output, and hemodynamic instability. Which intervention should the nurse anticipate implementing first?

C) Increase the current inotropic support to enhance cardiac output.

A) Administer a bolus of intravenous fluids to address hypotension.

B) Prepare for the administration of antiarrhythmic medication to manage PVCs.

C) Increase the current inotropic support to enhance cardiac output.

D) Notify the healthcare provider to discuss the initiation of temporary pacing.

A patient receiving potassium replacement therapy develops frequent premature ventricular contractions (PVCs), hypotension, and tachycardia. Which nursing intervention should the nurse prioritize to address the patient's hemodynamic instability?

C) Prepare for the administration of an antiarrhythmic medication after consulting with the healthcare provider.

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

B) Administer a bolus of intravenous fluids to improve blood pressure.

C) Prepare for the administration of an antiarrhythmic medication after consulting with the healthcare provider.

D) Request a stat echocardiogram to assess for potential cardiac tamponade.

A patient with a recent myocardial infarction is experiencing hemodynamic instability, including irregular heart rates, low blood pressure, and reduced ejection fraction. Despite antiarrhythmic medication and inotropic support, the condition is worsening. Which intervention should the nurse anticipate as the next step to stabilize the patient's condition?

B) Prepare for the insertion of an intra-aortic balloon pump

A) Administer an additional dose of antiarrhythmic medication

B) Prepare for the insertion of an intra-aortic balloon pump

C) Increase the dose of inotropic medication

D) Initiate high-flow oxygen therapy

A patient with myocardial infarction is experiencing hemodynamic instability, characterized by alternating tachycardia and bradycardia, hypotension, and metabolic acidosis. Despite adjustments in medication, the patient's condition continues to deteriorate. Which intervention should the nurse prioritize to stabilize the patient's hemodynamic status?

C) Prepare for the insertion of an intra-aortic balloon pump to augment cardiac function.

A) Administer an additional dose of inotropic medication to improve cardiac output.

B) Increase the infusion rate of intravenous fluids to address hypotension.

C) Prepare for the insertion of an intra-aortic balloon pump to augment cardiac function.

D) Initiate external pacing to manage the irregular heart rate.

Myocardial infarction - Nursing Case Study

Pathophysiology

• Primary mechanism: Myocardial infarction primarily occurs due to the rupture of an atherosclerotic plaque in the coronary artery, leading to thrombus formation and subsequent occlusion. This blockage significantly reduces blood flow, causing ischemia and necrosis of cardiac tissue.

• Secondary mechanism: The ischemic environment triggers a cascade of cellular changes, including calcium overload and reactive oxygen species production, further exacerbating tissue damage and impairing myocardial contractility.

• Key complication: If left untreated, the infarcted area can lead to complications such as heart failure, arrhythmias, or ventricular rupture, emphasizing the need for prompt intervention to restore blood flow and minimize cardiac damage.

Patient Profile

Demographics:

58-year-old male, construction worker

History:

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

• Current medications: Metformin, Lisinopril, Atorvastatin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Severe chest pain radiating to the left arm

• Key symptoms: Shortness of breath, nausea, diaphoresis, dizziness

• Vital signs: Blood pressure 160/100 mmHg, heart rate 110 bpm, respiratory rate 24 breaths per minute, temperature 98.6°F, oxygen saturation 91% on room air

Section 1

The initial assessment reveals significant findings consistent with an acute myocardial infarction. His electrocardiogram (ECG) shows ST-segment elevation in leads II, III, and aVF, indicative of an inferior wall myocardial infarction. Cardiac biomarkers are markedly elevated, with a troponin I level of 5.0 ng/mL (normal <0.04 ng/mL), confirming myocardial injury. The patient is diaphoretic, and his skin is cool and clammy to the touch, suggesting sympathetic nervous system activation due to acute cardiac distress. Lung auscultation reveals bibasilar crackles, raising concerns for potential pulmonary congestion secondary to left ventricular dysfunction.

The patient is administered aspirin and a high-dose statin as part of the acute coronary syndrome protocol. Nitroglycerin is given to alleviate chest pain, although the patient's blood pressure necessitates careful titration to avoid hypotension. Despite these interventions, his chest pain persists, and his oxygen saturation remains borderline at 92% with supplemental oxygen. His heart rate increases to 120 bpm, and premature ventricular contractions are noted on the cardiac monitor, highlighting the risk of arrhythmias.

Given these developments, a decision is made to proceed with emergent percutaneous coronary intervention (PCI) to restore coronary blood flow. The nursing team prepares the patient for transfer to the catheterization lab, ensuring continuous cardiac monitoring and intravenous access. The unfolding case raises critical questions about the management of potential complications, such as arrhythmias or heart failure, and underscores the need for vigilant assessment and timely intervention to mitigate further cardiac compromise.

Section 2

As the patient is transferred to the catheterization lab, the nursing team remains alert to any changes in his condition. During the procedure, the interventional cardiologist identifies a critical occlusion in the right coronary artery, confirming the diagnosis of an inferior wall myocardial infarction. A drug-eluting stent is successfully placed to restore blood flow. However, shortly after the procedure, the patient experiences a sudden drop in blood pressure to 85/60 mmHg and an increase in heart rate to 130 bpm. His skin becomes more diaphoretic, and he reports a sensation of worsening dyspnea. The cardiac monitor now shows frequent premature ventricular contractions, with episodes of non-sustained ventricular tachycardia, raising concerns about electrical instability.

In response to these changes, the healthcare team initiates a thorough reassessment. The findings suggest that the patient is developing cardiogenic shock, likely due to the compromised function of the left ventricle exacerbated by the myocardial infarction. Arterial blood gas analysis reveals a pH of 7.30, PaCO2 of 50 mmHg, and PaO2 of 60 mmHg, indicating respiratory acidosis and hypoxemia. A bedside echocardiogram is performed and shows reduced left ventricular ejection fraction at 30%, with impaired movement of the inferior wall of the heart.

The clinical team decides to optimize the patient's hemodynamic status by initiating an intravenous infusion of a vasopressor to support blood pressure and inotropic agents to enhance cardiac output. Diuretics are considered to manage fluid overload, evidenced by the persistent crackles in the lung bases. As these interventions are implemented, the nursing team closely monitors the patient's response, understanding that they must be vigilant for any further complications, such as worsening heart failure or arrhythmias, that could necessitate advanced cardiac support. This critical juncture emphasizes the importance of continuous assessment and precise clinical reasoning to navigate this complex phase of the patient's journey.

Section 3

As the interventions are administered, the nursing team observes the patient's response with heightened vigilance. Over the next few hours, the patient's blood pressure begins to stabilize, with readings improving to 100/70 mmHg, and the heart rate decreases slightly to 115 bpm. However, the patient continues to exhibit signs of respiratory distress, with an increased work of breathing and persistent crackles upon auscultation. The decision to administer diuretics proves beneficial, as evidenced by an increase in urine output and a slight reduction in lung crackles, suggesting a decrease in pulmonary congestion. Despite these positive changes, the patient remains in a tenuous state, requiring ongoing close monitoring.

New diagnostic results are brought to the team's attention, adding another layer to the clinical picture. A repeat arterial blood gas analysis shows slight improvement but still indicates metabolic acidosis with a pH of 7.35, PaCO2 of 45 mmHg, and PaO2 of 65 mmHg. Laboratory tests reveal elevated cardiac biomarkers, including Troponin I, confirming ongoing myocardial damage. Electrolyte imbalances are also noted, with hypokalemia identified as a potential contributor to the patient's arrhythmias. These findings prompt the team to initiate potassium replacement therapy while continuing to adjust the vasopressor and inotropic support as needed.

As the patient navigates this critical phase, the nursing team remains acutely aware of the potential for further complications, such as worsening heart failure or additional arrhythmias, which may necessitate the consideration of mechanical circulatory support. The integration of these new diagnostic insights emphasizes the importance of dynamic clinical reasoning, as the team works collaboratively to anticipate and address potential complications while striving to stabilize the patient's condition. This careful balancing act will guide the next steps in this complex case, focusing on achieving optimal outcomes in the face of evolving challenges.

Section 4

As the patient progresses through this critical phase, the nursing team observes a change in the patient's status that warrants immediate attention. Approximately four hours after the initiation of potassium replacement therapy, the patient's telemetry monitor alarms, indicating a new onset of ventricular ectopy, including frequent premature ventricular contractions (PVCs). Concurrently, the patient begins to exhibit signs of decreased cardiac output, with a sudden drop in blood pressure to 85/55 mmHg and an increase in heart rate to 130 bpm. The patient also reports increased chest discomfort and appears diaphoretic and anxious, raising concerns about the stability of the cardiac condition.

These developments prompt the nursing and medical teams to reassess their current management strategy. A focused cardiac examination reveals an irregular rhythm with diminished peripheral pulses, while auscultation continues to reveal persistent crackles, albeit less pronounced than before. Repeat laboratory tests show a slight improvement in potassium levels, though they remain on the lower side of normal, at 3.5 mmol/L. Given the patient's arrhythmias and hemodynamic instability, the team considers escalating the level of care, possibly by initiating an antiarrhythmic medication to manage the PVCs and further titrating the current inotropic support to enhance cardiac output.

The unfolding scenario underscores the critical need for dynamic clinical reasoning and the ability to adjust interventions in real-time. The team contemplates the potential necessity for advanced interventions, such as temporary pacing or even mechanical circulatory support, should the patient's condition continue to deteriorate. As they navigate these complex clinical decisions, the team remains committed to closely monitoring the patient's response to each adjustment, aiming to stabilize the cardiovascular system while preventing further myocardial damage. This vigilant approach will be pivotal in determining the next steps in the patient's care journey, focusing on achieving the most favorable outcomes amid evolving challenges.

Section 5

As the nursing and medical teams continue to monitor the patient’s condition, they initiate an antiarrhythmic medication to address the frequent PVCs and adjust the inotropic support to improve cardiac output. However, despite these interventions, the patient's condition shows signs of further deterioration. Approximately one hour after these adjustments, the patient’s heart rate becomes increasingly irregular, with episodes of tachycardia alternating with bradycardia. The blood pressure remains critically low at 80/50 mmHg, and the patient appears increasingly lethargic and confused, suggesting worsening cerebral perfusion.

In response to these alarming changes, an urgent echocardiogram is performed, revealing a marked decrease in left ventricular ejection fraction, now estimated at 25%, indicating significant impairment of cardiac contractility. Additionally, new laboratory results indicate a rising troponin level, consistent with ongoing myocardial injury, and metabolic acidosis with a blood pH of 7.32, reflecting poor tissue perfusion and oxygenation. The presence of metabolic acidosis, coupled with the evolving rhythm disturbances and hemodynamic instability, prompts the team to consider the need for mechanical circulatory support, such as an intra-aortic balloon pump, to augment cardiac function and stabilize the patient's condition.

Recognizing the complexity of the situation, the team engages in a thorough clinical reasoning process, weighing the risks and benefits of advanced interventions. They prioritize continuous monitoring and reassessment, ensuring that any new changes in the patient’s status are promptly addressed. As the patient’s journey unfolds, the team remains vigilant, ready to escalate care to prevent further complications and optimize outcomes in this critical phase of myocardial infarction management.