A patient with a history of myocardial infarction is experiencing increased respiratory distress, bilateral crackles, and an S3 heart sound. The patient is on 4 L/min of oxygen via nasal cannula and has been started on IV furosemide. Which nursing intervention is most appropriate to further address the patient's respiratory status?

B) Position the patient in high Fowler's position.

A) Increase the oxygen flow rate to 6 L/min via nasal cannula.

B) Position the patient in high Fowler's position.

C) Administer a second dose of furosemide immediately.

D) Prepare for intubation and mechanical ventilation.

A patient with suspected heart failure is experiencing increased respiratory distress, bilateral crackles extending to the mid-lung fields, and decreasing oxygen saturation despite supplemental oxygen. Which of the following interventions is most appropriate to address the patient’s respiratory and fluid status?

B) Administer intravenous furosemide and increase oxygen to 4 L/min via nasal cannula

A) Increase supplemental oxygen to 10 L/min via non-rebreather mask

B) Administer intravenous furosemide and increase oxygen to 4 L/min via nasal cannula

C) Initiate high-flow nasal cannula therapy and prepare for intubation

D) Start continuous positive airway pressure (CPAP) therapy and reduce fluid intake

A patient with an anterior STEMI has been prepared for primary percutaneous coronary intervention (PCI). Which nursing intervention is most critical to perform prior to the patient's transfer to the catheterization lab?

C) Verify the patient has received dual antiplatelet therapy and intravenous heparin.

A) Administer a bolus of intravenous fluids to ensure adequate hydration.

B) Educate the patient and family about the PCI procedure and expected outcomes.

C) Verify the patient has received dual antiplatelet therapy and intravenous heparin.

D) Apply continuous cardiac monitoring to detect any potential arrhythmias.

A patient with an anterior STEMI is being prepared for primary PCI. The nurse must prioritize which of the following actions to prevent complications associated with this condition?

B) Monitor the patient for signs of bleeding after dual antiplatelet therapy.

A) Administer a beta-blocker to control heart rate.

B) Monitor the patient for signs of bleeding after dual antiplatelet therapy.

C) Position the patient upright to reduce cardiac workload.

D) Prepare the patient for immediate thrombolytic therapy.

A patient with anterior STEMI is being prepared for primary PCI but begins to show signs of hemodynamic instability, including hypotension, tachycardia, and pulmonary congestion. Which of the following nursing interventions is most critical to perform immediately to manage the patient's condition?

C) Initiate intravenous inotropic support to enhance cardiac output.

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

B) Administer a stat dose of diuretic to reduce pulmonary congestion.

C) Initiate intravenous inotropic support to enhance cardiac output.

D) Position the patient in Trendelenburg to improve perfusion.

A patient with anterior STEMI is exhibiting signs of hemodynamic instability, including hypotension and tachycardia, with crackles in lung bases. Given the patient's clinical presentation and recent lab findings of a potassium level of 3.2 mEq/L, which nursing intervention should be prioritized to prevent further cardiac complications?

B) Administer a potassium supplement to correct the electrolyte imbalance.

A) Increase the rate of dobutamine infusion to address hypotension.

B) Administer a potassium supplement to correct the electrolyte imbalance.

C) Initiate continuous positive airway pressure (CPAP) therapy to reduce pulmonary congestion.

D) Prepare for immediate defibrillation in anticipation of ventricular fibrillation.

A patient with an extensive anterior wall STEMI is displaying signs of cardiogenic shock, including confusion, restlessness, and decreased urine output. Based on this clinical presentation, which nursing intervention is the priority to stabilize the patient?

C) Prepare the patient for immediate PCI to restore coronary perfusion.

A) Increase the dose of dobutamine to improve cardiac output.

B) Administer a diuretic to reduce pulmonary congestion.

C) Prepare the patient for immediate PCI to restore coronary perfusion.

D) Initiate a fluid bolus to improve renal perfusion.

A patient with an anterior wall STEMI is exhibiting confusion, decreased urine output, and elevated BNP levels. What is the priority nursing intervention to address these symptoms?

C) Prepare the patient for immediate PCI

A) Administer a bolus of intravenous fluids

B) Increase the dose of dobutamine

C) Prepare the patient for immediate PCI

D) Administer a diuretic to reduce pulmonary congestion

A patient with worsening cardiogenic shock is being monitored in the ICU. Despite treatment, the patient's condition includes hypotension, tachycardia, and signs of peripheral hypoperfusion. Which intervention should the nurse prioritize to address the underlying issue of reduced cardiac output?

C) Prepare the patient for percutaneous coronary intervention (PCI).

A) Increase the rate of dobutamine infusion to enhance cardiac contractility.

B) Administer a bolus of normal saline to improve preload.

C) Prepare the patient for percutaneous coronary intervention (PCI).

D) Initiate a high-dose norepinephrine infusion to raise blood pressure.

A patient with cardiogenic shock is exhibiting signs of worsening pulmonary edema and peripheral hypoperfusion despite dobutamine infusion. Which nursing intervention should be prioritized to support the patient's hemodynamic status?

B) Prepare for potential initiation of mechanical circulatory support

A) Increase the rate of oxygen supplementation to improve oxygen saturation

B) Prepare for potential initiation of mechanical circulatory support

C) Administer an additional bolus of intravenous fluids to improve blood pressure

D) Educate the patient on the importance of adhering to fluid restrictions

MI with focus on abnormal physical exam, abnormal labs, ECG for STEMI and NSTEMI - Nursing Case Study

Pathophysiology

• Primary mechanism: Coronary artery blockage due to atherosclerotic plaque rupture leads to reduced blood flow, causing myocardial ischemia. In STEMI, complete blockage results in ST elevation, whereas in NSTEMI, partial blockage causes ST depression or T-wave inversion.

• Secondary mechanism: Myocyte death and release of cardiac biomarkers (troponin) into the bloodstream indicate myocardial necrosis. Elevated troponin levels confirm myocardial injury, distinguishing MI from other chest pain causes.

• Key complication: Impaired contractility due to myocardial damage may cause abnormal heart sounds (S3, S4), pulmonary crackles, or hypotension. Rapid identification and treatment are critical to prevent heart failure and arrhythmias.

Patient Profile

Demographics:

58-year-old male, construction worker

History:

• Key past medical history: Hypertension, hyperlipidemia, smoker (20 pack-year history)

• Current medications: Lisinopril, atorvastatin, aspirin

• Allergies: Penicillin

Current Presentation:

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

• Key symptoms: Dyspnea, diaphoresis, nausea, lightheadedness

• Vital signs: Blood pressure 150/95 mmHg, heart rate 110 bpm, respiratory rate 24 breaths/min, temperature 37.2°C, oxygen saturation 92% on room air

Abnormal Physical Exam:

• S3 heart sound, jugular venous distension, bilateral crackles in lung bases

Abnormal Labs:

• Elevated troponin I

• Elevated CK-MB

• Elevated LDL cholesterol

ECG Findings:

• STEMI: ST elevation in leads II, III, and aVF

• NSTEMI: ST depression and T-wave inversion in leads V4-V6

Complications:

• Developing heart failure

• Possible pulmonary edema

Section 1

Change in Patient Status:

Shortly after the initial assessment, the patient’s condition began to deteriorate further. He developed increasing respiratory distress, with oxygen saturation dropping to 88% despite being on supplemental oxygen at 2 L/min via nasal cannula. His respiratory rate increased to 30 breaths per minute, and he appeared visibly anxious and fatigued. Auscultation of the lungs revealed worsening bilateral crackles, now extending to the mid-lung fields, indicating likely progression towards pulmonary edema. This change in status suggests that the heart's ability to effectively pump blood is compromised, leading to fluid accumulation in the lungs.

In response to these findings, the medical team promptly increased the oxygen delivery to 4 L/min and initiated diuretic therapy with intravenous furosemide to address the fluid overload. Additionally, the patient's blood pressure was noted to have decreased to 135/88 mmHg, potentially reflecting a reduction in cardiac output as the heart struggles to maintain effective circulation. This hypotensive trend, along with the presence of an S3 heart sound and jugular venous distension, reinforces the likelihood of developing heart failure, necessitating close monitoring and possible escalation of care.

The patient’s clinical course underscores the need for immediate and effective interventions to stabilize his condition and prevent further complications such as cardiogenic shock or arrhythmias. The team is considering further diagnostic imaging, such as an echocardiogram, to assess cardiac function and structure more comprehensively, which will guide ongoing treatment decisions. This situation highlights the importance of timely identification and management of acute myocardial infarction complications to improve patient outcomes.

Section 2

As the medical team continued to monitor the patient, new diagnostic results became available, providing crucial insights into his deteriorating condition. The ECG revealed significant ST-segment elevations in the anterior leads, consistent with an anterior ST-Elevation Myocardial Infarction (STEMI). Additionally, there were Q waves forming, indicating an evolving myocardial infarction. Cardiac biomarkers, including troponin I, were markedly elevated at 12 ng/mL (normal <0.04 ng/mL), further confirming myocardial injury. The echocardiogram showed reduced left ventricular ejection fraction at 35%, with hypokinesis of the anterior wall, suggesting impaired cardiac function.

These findings prompted the medical team to urgently initiate reperfusion therapy. Given the high-risk nature of an anterior STEMI and the patient's unstable condition, primary percutaneous coronary intervention (PCI) was prioritized. The patient was prepared for immediate transfer to the catheterization lab. Concurrently, dual antiplatelet therapy with aspirin and clopidogrel, alongside intravenous heparin, was administered to prevent further thrombus formation.

The diagnostic results underscored the severity of the patient's condition and the pressing need for intervention to restore coronary perfusion. The clinical team also anticipated potential complications such as arrhythmias or further hemodynamic instability. As preparations for PCI proceeded, the focus remained on stabilizing the patient while minimizing risks associated with the procedure. These steps were critical in addressing the underlying cause of the myocardial infarction and preventing progression to cardiogenic shock or life-threatening arrhythmias, thereby charting the course for the next phase of the patient's treatment journey.

Section 3

As the medical team initiated the transfer to the catheterization lab for primary PCI, they closely monitored the patient's vital signs and overall status. Despite the swift intervention, the patient began exhibiting signs of hemodynamic instability. His blood pressure dropped to 85/50 mmHg, and he developed tachycardia with a heart rate of 120 beats per minute. Auscultation revealed new-onset crackles at the lung bases, suggesting pulmonary congestion. These changes indicated a potential progression towards cardiogenic shock, necessitating immediate attention.

In response to this deterioration, the team initiated intravenous inotropic support with dobutamine, aiming to improve cardiac output and stabilize blood pressure. Concurrently, oxygen therapy was administered to address hypoxia, as the patient's oxygen saturation had decreased to 89% on room air. Continuous ECG monitoring was crucial, given the increased risk of arrhythmias, especially in the context of anterior STEMI. The medical team was vigilant for any signs of ventricular tachycardia or fibrillation, which could pose immediate life-threatening risks.

Laboratory values were revisited to assess the patient's metabolic status and guide further management. The latest arterial blood gas analysis revealed a mild metabolic acidosis with a pH of 7.32, bicarbonate level of 18 mEq/L, and lactate level of 3.5 mmol/L, indicative of tissue hypoperfusion. Electrolyte imbalances were also noted, with a potassium level of 3.2 mEq/L, necessitating cautious correction to prevent exacerbation of arrhythmic potential. These clinical findings underscored the need for rapid PCI to restore coronary blood flow and prevent further cardiac compromise, while also highlighting the critical importance of ongoing supportive measures to stabilize the patient's condition.

Section 4

As the patient was being prepared for the catheterization lab, the nursing team observed new diagnostic results that warranted immediate attention. The repeated ECG showed significant ST elevation in leads V2 to V4, confirming an extensive anterior wall STEMI. In addition, there were concerning changes suggesting early Q wave formation, indicative of myocardial necrosis. These findings reinforced the urgency of rapid intervention to limit myocardial damage.

Laboratory tests returned with a troponin I level markedly elevated at 12 ng/mL, confirming ongoing myocardial injury. The BNP level was also elevated at 500 pg/mL, correlating with the clinical signs of heart failure, such as pulmonary congestion and reduced cardiac output. In light of these results, the medical team increased the dose of dobutamine to optimize hemodynamic support, while carefully titrating potassium replacement to maintain a target level of 4 mEq/L, thereby reducing the risk of arrhythmias.

Despite these interventions, the patient's condition continued to evolve. The patient developed mild confusion and restlessness, suggestive of decreased cerebral perfusion. His urine output decreased to 20 mL/hour, indicating worsening renal perfusion. These changes highlighted the multi-organ impact of cardiogenic shock and underscored the importance of prompt PCI to reestablish coronary perfusion. The team continued to monitor the patient closely, prepared to escalate supportive care measures as needed to stabilize his condition and prevent further complications.

Section 5

As the team continued to manage the patient, new complications began to unfold. The patient's blood pressure dropped to 85/50 mmHg, prompting concerns about worsening cardiogenic shock. Heart rate remained elevated at 110 beats per minute, and despite the increased dobutamine infusion, signs of peripheral hypoperfusion, such as cool and clammy skin, became more pronounced. The patient's oxygen saturation decreased to 88% on 4 liters of supplemental oxygen, and auscultation revealed crackles in both lung bases, indicating worsening pulmonary edema.

In response to these developments, the medical team initiated a low-dose norepinephrine infusion to support blood pressure and improve coronary perfusion. At the same time, they increased diuretics to manage fluid overload, carefully balancing the risk of further renal impairment given the reduced urine output. Repeat laboratory tests showed a further increase in troponin I to 15 ng/mL, suggesting ongoing myocardial injury, while kidney function tests revealed a rising creatinine level of 2.2 mg/dL, confirming acute kidney injury.

These findings prompted a multidisciplinary discussion focusing on the need for more aggressive hemodynamic support and the potential for mechanical circulatory support if the patient's condition did not stabilize. The urgency of proceeding with percutaneous coronary intervention (PCI) was underscored, as revascularization remained the best hope for halting the cascade of multi-organ dysfunction. The team prepared for potential escalation, including the use of intra-aortic balloon pump or other advanced therapies, to optimize the patient's chances of recovery while closely monitoring for any further deterioration.