Acute MI - Nursing Case Study

Pathophysiology

• Primary mechanism: Acute Myocardial Infarction (MI) primarily occurs due to coronary artery occlusion, typically triggered by a ruptured atherosclerotic plaque. This rupture exposes thrombogenic substances, leading to platelet aggregation and thrombus formation, blocking the blood flow to the heart muscle.

• Secondary mechanism: Prolonged occlusion leads to ischemia, which, if not resolved, results in irreversible myocardial cell damage and necrosis. Ischemia induces anaerobic metabolism, causing acidosis and further damaging the myocardial cells.

• Key complication: Acute MI can result in complications such as arrhythmias due to electrical instability from ischemic myocardial tissue. Additionally, heart failure or cardiogenic shock may occur due to the loss of contractile function in the damaged myocardium.

Patient Profile

Demographics:

65-year-old male, retired construction worker

History:

• Key past medical history: Hypertension, Type II Diabetes, High cholesterol, History of smoking

• Current medications: Lisinopril, Metformin, Atorvastatin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Severe chest pain

• Key symptoms: Shortness of breath, fatigue, dizziness, nausea, and excessive sweating

• Vital signs: Blood pressure 170/100 mmHg, Heart rate 110 bpm, Respiratory rate 22 breaths per minute, Oxygen saturation 90% on room air, Temperature 37.5°C

Section 1

New Diagnostic Results:

The results of the patient's electrocardiogram (ECG) indicated ST-segment elevation in the anterior leads (V1-V4), suggesting an anterior wall ST-segment elevation myocardial infarction (STEMI). His blood work showed elevated troponin I levels at 0.5 ng/mL, further substantiating the diagnosis of acute MI. His blood glucose levels were also elevated at 200 mg/dL, indicating poor control of his diabetes. A lipid panel showed total cholesterol of 240 mg/dL, LDL cholesterol of 160 mg/dL, and HDL cholesterol of 35 mg/dL, confirming his history of hyperlipidemia.

Change in Patient Status:

Over the next few hours, the patient's condition started to deteriorate. His blood pressure dropped to 90/60 mmHg, and his heart rate increased to 120 bpm. His respiratory rate also increased to 28 breaths per minute, and oxygen saturation dropped to 88% on room air. The patient reported increasing chest pain and a feeling of impending doom. He also developed cold, clammy skin, indicating a decrease in peripheral perfusion due to worsening myocardial function. This change in status is concerning for the development of cardiogenic shock, a serious complication of acute MI.

Section 2

Response to Interventions:

In an attempt to stabilize the patient's deteriorating condition, immediate medical interventions were initiated. He was administered aspirin and a loading dose of clopidogrel to inhibit platelet aggregation, in addition to oxygen therapy to improve his oxygen saturation. Despite these interventions, the patient's chest pain persisted, and his oxygen saturation remained at 88%. A repeat ECG showed persistent ST-segment elevation. The patient was also started on an IV infusion of nitroglycerin to improve his coronary blood flow and reduce myocardial oxygen demand, but this led to further decrease in his blood pressure to 85/55 mmHg.

New Complications:

Given the persistent ST-segment elevation on ECG and lack of response to initial interventions, the patient was suspected of having a large anterior wall myocardial infarction that was not resolving. His falling blood pressure and increasing heart rate, despite nitroglycerin administration, suggested that he might be developing left ventricular failure, a serious complication of a large anterior MI. This was further supported by the appearance of crackles on auscultation of his lungs, indicating possible pulmonary edema. His capillary blood glucose level also increased to 250 mg/dL, suggesting that the stress of the acute illness was exacerbating his poorly controlled diabetes. The patient's condition was now critical, necessitating further urgent interventions and close monitoring.

Section 3

Change in Patient Status:

Despite aggressive medical interventions, the patient's condition continued to deteriorate. His blood pressure dropped further to 80/50 mmHg, while his heart rate increased to 120 bpm. The patient's breathing became more labored, and his oxygen saturation declined to 84% on 3L of oxygen via nasal cannula. On auscultation of his lungs, the crackles worsened, and his breath sounds were diminished at both bases. The patient's mental status also began to change; he became increasingly restless and anxious, displaying clear signs of air hunger.

New Diagnostic Results:

To understand the full extent of the patient's condition, further diagnostic tests were ordered. The repeat ECG showed deepening ST-segment elevations and new Q waves, indicative of an evolving anterior wall myocardial infarction. A chest X-ray revealed bilateral infiltrates, consistent with pulmonary edema. His troponin levels had risen to 3.5 ng/mL, further supporting the diagnosis of a myocardial infarction. Blood gas analysis revealed a PaO2 of 58 mmHg, PaCO2 of 47 mmHg, and a pH of 7.31, indicating the presence of acute respiratory acidosis. His blood glucose level remained elevated at 255 mg/dL despite insulin sliding scale therapy. These findings highlighted the severity of the patient's condition, necessitating a rapid escalation of care and potentially more invasive interventions.

Section 4

New Complications:

As the night progressed, the patient's condition took a turn for the worse. The patient’s blood pressure continued to drop, now reading 70/40 mmHg, and his heart rate climbed to 130 bpm. He became increasingly agitated, and his oxygen saturation levels further declined to 80% despite increasing the oxygen flow to 5L via nasal cannula. His restlessness and increased work of breathing indicated worsening hypoxia.

In addition, the patient began to complain of severe abdominal pain, which was not present before. On examination, his abdomen was distended and tender to touch, particularly in the right upper quadrant. The patient’s urine output also decreased significantly, to less than 30 ml/hr. Laboratory tests revealed an increase in liver enzymes, with an AST of 200 U/L and an ALT of 150 U/L. His creatinine level had also risen to 2.5 mg/dL, indicating possible acute kidney injury. This new development suggested that the patient's myocardial infarction might have led to secondary complications such as hypoxic liver injury and acute renal failure. These new complications required immediate attention and possible transfer to the intensive care unit for closer monitoring and advanced interventions.

Section 5

New Diagnostic Results:

Upon arrival in the ICU, the patient was immediately assessed by the on-duty intensivist, who ordered a series of diagnostic tests to further evaluate the patient's condition. An abdominal ultrasound was performed, revealing a distended gallbladder with possible gallstones. This could explain the severe right upper quadrant pain and the elevated liver enzymes. The intensivist also noted the patient's decreased urine output and elevated creatinine levels, and ordered a renal ultrasound as well, which showed signs of acute tubular necrosis - a common cause of acute kidney injury.

Meanwhile, the patient's EKG showed persistent ST segment elevation, suggesting that the myocardial infarction was not yet resolved. Blood samples were also sent to the lab for cardiac biomarkers, which showed a troponin level of 5.0 ng/mL, further confirming ongoing myocardial damage. These new diagnostic results painted a clearer picture of the patient's condition, but also meant that the patient was now dealing with multiple organ dysfunction syndrome (MODS) secondary to his myocardial infarction, a serious complication with a high mortality rate. This required a prompt and coordinated effort from the multidisciplinary team in the ICU to manage his cardiovascular, renal and gastrointestinal issues simultaneously.