A patient with a confirmed STEMI is experiencing worsening chest pain, shortness of breath, hypotension, and decreased oxygen saturation despite supplemental oxygen. Given these clinical findings, which intervention should the nurse anticipate as a priority to stabilize the patient?

B) Prepare for immediate percutaneous coronary intervention (PCI).

A) Administer a higher dose of intravenous nitroglycerin.

B) Prepare for immediate percutaneous coronary intervention (PCI).

C) Administer a fluid bolus to address hypotension.

D) Increase supplemental oxygen to 100% via non-rebreather mask.

A patient with a confirmed STEMI is experiencing worsening chest pain, hypotension, tachycardia, and pulmonary crackles. Despite receiving supplemental oxygen and intravenous nitroglycerin, the patient's oxygen saturation remains at 88%. Which of the following nursing interventions should be prioritized to stabilize the patient's condition?

C) Initiate an inotropic agent to improve cardiac output.

A) Increase the nitroglycerin infusion rate to improve coronary blood flow.

B) Administer a diuretic to reduce pulmonary congestion.

C) Initiate an inotropic agent to improve cardiac output.

D) Position the patient in Trendelenburg to increase blood pressure.

A patient with acute heart failure is experiencing increased respiratory distress and decreased oxygen saturation despite high-flow oxygen therapy. The latest echocardiogram shows a further decline in left ventricular ejection fraction to 25%. Which intervention should the nurse anticipate to address the patient's respiratory distress while also considering the current cardiac status?

B) Initiate non-invasive positive pressure ventilation

A) Administer a diuretic to reduce pulmonary congestion

B) Initiate non-invasive positive pressure ventilation

C) Increase the rate of intravenous fluids to improve renal perfusion

D) Prepare the patient for endotracheal intubation and mechanical ventilation

A patient with worsening heart failure is showing signs of acute pulmonary edema with increasing respiratory distress, despite high-flow oxygen therapy. The healthcare team is considering the use of dobutamine to enhance myocardial contractility. Which of the following nursing interventions should be prioritized to address the patient's current condition?

C) Initiate non-invasive positive pressure ventilation to improve oxygenation.

A) Elevate the head of the bed to 30-45 degrees to improve ventilation.

B) Administer a diuretic as prescribed to decrease fluid overload.

C) Initiate non-invasive positive pressure ventilation to improve oxygenation.

D) Prepare the patient for potential intubation due to respiratory failure.

A patient receiving dobutamine infusion for heart failure management develops frequent premature ventricular contractions (PVCs) and non-sustained ventricular tachycardia. Laboratory results indicate hypokalemia. What is the most appropriate nursing intervention to address these findings?

B) Administer intravenous potassium supplementation as ordered.

A) Increase the rate of dobutamine infusion to improve cardiac output.

B) Administer intravenous potassium supplementation as ordered.

C) Initiate a continuous infusion of magnesium sulfate.

D) Apply external defibrillation pads in anticipation of potential cardiac arrest.

A patient with a suspected inferior STEMI is being prepared for percutaneous coronary intervention (PCI). The nurse notes a slight drop in blood pressure to 90/55 mmHg following the initiation of dobutamine infusion. What is the most appropriate nursing action to optimize the patient's cardiac output without increasing myocardial oxygen consumption?

D) Maintain the current dobutamine rate and closely monitor hemodynamic status

A) Increase the rate of dobutamine infusion

B) Administer intravenous fluids to increase preload

C) Position the patient in Trendelenburg position

D) Maintain the current dobutamine rate and closely monitor hemodynamic status

A patient with an evolving inferior STEMI is being prepared for percutaneous coronary intervention (PCI). Which nursing intervention is most critical to address the patient's slight drop in blood pressure while ensuring myocardial oxygen demand is not exacerbated?

D) Titrate the dobutamine infusion to optimize cardiac output.

A) Increase the rate of the dobutamine infusion.

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

C) Administer additional intravenous fluids to increase blood volume.

D) Titrate the dobutamine infusion to optimize cardiac output.

A patient in the catheterization lab exhibits signs of cardiogenic shock with an elevated heart rate, decreased blood pressure, and confusion. The nurse notes persistent ST-elevation in the inferior leads and right ventricular involvement on a right-sided ECG. Given these findings, which nursing intervention is most critical to implement immediately?

B) Increase the rate of dobutamine infusion to improve cardiac output

A) Administer intravenous fluids aggressively to increase preload

B) Increase the rate of dobutamine infusion to improve cardiac output

C) Prepare the patient for emergent intubation to manage respiratory distress

D) Administer a beta-blocker to control the heart rate and decrease myocardial oxygen demand

A patient in the catheterization lab presents with an increased heart rate of 120 beats per minute, blood pressure of 85/50 mmHg, dyspnea, and mild confusion. The nursing team suspects cardiogenic shock. Which of the following interventions should the nurse prioritize to stabilize the patient's hemodynamic status?

B) Increase the rate of the dobutamine infusion to support myocardial contractility.

A) Administer a bolus of normal saline to increase preload.

B) Increase the rate of the dobutamine infusion to support myocardial contractility.

C) Prepare the patient for immediate intubation and mechanical ventilation.

D) Administer a dose of nitroglycerin to relieve potential chest pain.

MI focus on STEMI and NSTEMI on ECG , abnormal S & Sm and abnormal labs - Nursing Case Study

Pathophysiology

• Primary mechanism: In STEMI, complete coronary artery occlusion leads to transmural ischemia, which results in ST-segment elevation on ECG due to full-thickness myocardial injury.

• Secondary mechanism: NSTEMI involves partial coronary artery occlusion, causing subendocardial ischemia and ST-segment depression or T-wave inversion on ECG, reflecting partial-thickness myocardial damage.

• Abnormal S & Sm: Reduced systolic (S) and diastolic (Sm) myocardial velocities on echocardiography indicate impaired myocardial contractility and relaxation due to ischemic injury.

• Key lab findings: Elevated cardiac biomarkers (e.g., troponin) confirm myocardial necrosis, differentiating MI from angina and reflecting the extent of myocardial cell death.

• Key complication: Both STEMI and NSTEMI can lead to heart failure, arrhythmias, or cardiogenic shock if not promptly managed, emphasizing the importance of timely intervention.

Patient Profile

Demographics:

56-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, diaphoresis, nausea, dizziness

• Vital signs: Blood pressure 150/95 mmHg, heart rate 110 bpm, respiratory rate 24 breaths per minute, temperature 37.8°C, oxygen saturation 92% on room air

Section 1

As the healthcare team continues to assess the patient's condition, new diagnostic results provide crucial insights into the severity of his myocardial infarction. The 12-lead ECG reveals significant ST-segment elevation in the anterior leads, confirming a diagnosis of STEMI. Additionally, there is marked ST-segment depression in the inferior leads, indicating reciprocal changes. This suggests a significant ischemic event affecting the left anterior descending artery. An echocardiogram shows reduced systolic and diastolic myocardial velocities, particularly in the anterior wall, highlighting impaired myocardial contractility and relaxation. These findings correlate with the patient's elevated troponin levels, which are measured at 0.5 ng/mL initially and rise to 12 ng/mL within 6 hours, confirming extensive myocardial injury.

Shortly after these diagnostic revelations, the patient's status changes, marked by increasing chest pain and worsening shortness of breath. His blood pressure drops to 90/60 mmHg, while his heart rate remains elevated at 120 bpm. Oxygen saturation decreases to 88% despite supplemental oxygen, and pulmonary crackles are now audible upon auscultation, suggesting the development of acute heart failure. These changes necessitate immediate clinical reasoning to adjust treatment strategies, focusing on stabilizing hemodynamics and relieving myocardial strain.

The team quickly escalates care, administering intravenous nitroglycerin to alleviate chest pain and improve coronary blood flow. However, the patient's hypotension complicates this approach, requiring careful titration and potential consideration of inotropic support to maintain adequate cardiac output. Continuous monitoring and reassessment are vital as the team anticipates potential complications such as arrhythmias or cardiogenic shock. The unfolding scenario underscores the need for timely interventions and dynamic clinical decision-making to prevent further deterioration in this patient experiencing a life-threatening STEMI.

Section 2

In the midst of these acute developments, the healthcare team observes a critical change in the patient's status. Despite the initial relief from chest pain following intravenous nitroglycerin administration, the patient begins to exhibit signs of increasing respiratory distress. His respiratory rate escalates to 28 breaths per minute, and his oxygen saturation further declines to 85% even with high-flow oxygen therapy. As the team reassesses, they note that the pulmonary crackles have intensified, and the patient is now experiencing orthopnea, indicating worsening pulmonary congestion and potential progression to acute pulmonary edema.

In response to these concerning signs, the team conducts a repeat echocardiogram, which reveals further decline in left ventricular function, with an ejection fraction now estimated at 25%. This significant reduction in cardiac output is corroborated by new laboratory results showing a BNP level elevated at 1500 pg/mL, suggesting exacerbated heart failure. Furthermore, the patient's renal function tests indicate a rise in creatinine from 1.0 to 1.6 mg/dL, hinting at renal hypoperfusion secondary to decreased cardiac output.

These findings prompt the team to reconsider their management strategy, weighing the risks and benefits of introducing inotropic support, such as dobutamine, to enhance myocardial contractility. Careful clinical reasoning is required to balance the goal of improving cardiac output against the risk of exacerbating myocardial oxygen demand. The team also considers the implementation of non-invasive positive pressure ventilation to alleviate respiratory distress and improve oxygenation. As they navigate these complex decisions, the healthcare team remains vigilant for signs of further complications, such as arrhythmias, which could indicate worsening myocardial instability. This dynamic situation underscores the necessity for ongoing monitoring and adaptation of the treatment plan to optimize patient outcomes.

Section 3

As the healthcare team implements non-invasive positive pressure ventilation, the patient's oxygen saturation improves modestly to 88%. Despite this slight improvement, the patient remains in significant distress, and the decision is made to initiate dobutamine infusion at a low dose to support cardiac output without excessively increasing myocardial oxygen demand. Close monitoring of the patient's hemodynamic status is initiated, with frequent reassessment of vital signs and cardiac rhythm.

Within an hour of starting dobutamine, the patient's heart rate increases to 110 beats per minute, and blood pressure stabilizes at 100/60 mmHg. However, new diagnostic results reveal alarming changes: the ECG now shows frequent premature ventricular contractions (PVCs) and occasional runs of non-sustained ventricular tachycardia, raising concerns about the risk of sustained arrhythmias. This development necessitates a thorough evaluation of the patient's electrolyte levels, which reveal hypokalemia with a potassium level of 3.2 mmol/L, likely exacerbated by diuretic therapy and renal impairment.

The team promptly addresses the hypokalemia with intravenous potassium supplementation, aiming to mitigate the risk of arrhythmias. As the patient's clinical picture evolves, the focus shifts to maintaining a delicate balance between aggressive management of heart failure and careful monitoring for arrhythmic complications. The healthcare team remains vigilant, understanding that further deterioration could necessitate more invasive interventions, such as mechanical circulatory support, to stabilize the patient's condition and prevent further decline.

Section 4

As the healthcare team continues to closely monitor the patient, a new complication arises. Despite the correction of hypokalemia, the patient's ECG shows further deterioration with the development of ST-elevation in leads II, III, and aVF, suggesting an evolving inferior STEMI. This new finding is concerning, as it indicates acute myocardial injury that requires immediate intervention to restore coronary perfusion and minimize myocardial damage. Simultaneously, the patient's cardiac biomarkers, including troponin I, have markedly increased, reinforcing the diagnosis of an acute myocardial infarction.

In response to these changes, the team initiates antiplatelet therapy with aspirin and clopidogrel, alongside anticoagulation with heparin, aiming to prevent further thrombotic complications. Additionally, a decision is made to prepare the patient for percutaneous coronary intervention (PCI) to open the occluded coronary artery and restore perfusion. During this preparation, the patient's vital signs are meticulously monitored, revealing a slight drop in blood pressure to 90/55 mmHg, which is managed by adjusting the dobutamine infusion to optimize cardiac output without exacerbating myocardial oxygen consumption.

As the patient is stabilized for transfer to the catheterization lab, the healthcare team reflects on the importance of timely intervention in the setting of a STEMI and the need for ongoing vigilance to detect any further complications. They recognize that while the immediate focus is on revascularization, continued monitoring for heart failure symptoms and arrhythmic events remains critical in the post-intervention phase. This case underscores the complexity of managing acute coronary syndromes, especially when compounded by pre-existing conditions and treatment-related side effects, necessitating a coordinated multidisciplinary approach to optimize patient outcomes.

Section 5

As the patient is transferred to the catheterization lab, the healthcare team remains alert to potential new complications. Despite initial stabilization, the patient exhibits a sudden change in status shortly after arrival. The nursing staff notes an increase in the patient's heart rate to 120 beats per minute, accompanied by a further drop in blood pressure to 85/50 mmHg. The patient begins to exhibit signs of dyspnea and mild confusion, suggesting a possible progression towards cardiogenic shock. These symptoms prompt an urgent reassessment of the patient's hemodynamic status and a review of the ongoing dobutamine infusion, which is temporarily increased to enhance myocardial contractility and support blood pressure.

Simultaneously, new diagnostic results from repeat laboratory tests reveal a significant rise in creatine kinase-MB (CK-MB) levels, in addition to the already elevated troponin I, further confirming the extent of myocardial injury. This biochemical evidence aligns with the clinical presentation and reinforces the necessity for rapid revascularization. Moreover, the ECG is re-evaluated and shows persistent ST-elevation in the inferior leads, with reciprocal changes in the anterior leads, confirming the diagnosis of an inferior STEMI with potential right ventricular involvement.

Acknowledging the gravity of the situation, the cardiology team swiftly performs a right-sided ECG, which reveals ST elevation in lead V4R, indicating right ventricular infarction. This finding necessitates careful fluid management to maintain right-sided preload, highlighting the importance of balancing inotropic support with cautious volume resuscitation. The team proceeds with PCI, successfully restoring perfusion to the inferior and right coronary arteries. Post-intervention, the patient's vital signs stabilize, with a gradual improvement in blood pressure and mental status. This outcome reflects the critical value of timely and coordinated intervention in managing complex acute coronary syndromes and sets the stage for ongoing post-procedural care focused on preventing recurrent ischemic events and supporting cardiac recovery.