Acute MI - Nursing Case Study

Pathophysiology

• Primary Mechanism: Acute myocardial infarction (MI) usually results from a sudden obstruction of blood flow in the coronary arteries. This often occurs due to the rupture of an atherosclerotic plaque, leading to thrombus formation and subsequent vessel occlusion. Without blood, the heart muscle becomes ischemic and starts to die.

• Secondary Mechanism: When a significant portion of the heart muscle is deprived of oxygen, this leads to the release of substances such as troponins and creatine kinase-MB (CK-MB) into the bloodstream. High levels of these markers are used to diagnose an acute MI.

• Key Complication: The most immediate risk is life-threatening arrhythmias, such as ventricular fibrillation, caused by the disruption of the electrical pathways in the heart. Other complications can include heart failure, due to the loss of pumping action from the damaged heart muscle, and cardiogenic shock, a severe drop in blood pressure that impairs vital organ perfusion.

Patient Profile

Demographics:

62-year-old male, retired construction worker

History:

• Key past medical history: Hypertension, Type 2 Diabetes, previous episode of unstable angina

• Current medications: Metformin, Lisinopril, Aspirin

• Allergies: Penicillin

Current Presentation:

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

• Key symptoms: Shortness of breath, nausea, sweating, fatigue, irregular heartbeat

• Vital signs: Blood pressure 160/95 mmHg, pulse 110 bpm, respiratory rate 24 breaths per minute, temperature 98.6 F, oxygen saturation 90% on room air

Section 1

New Diagnostic Results:

The patient's EKG shows signs of ST-segment elevation in leads II, III, and aVF, which is indicative of an inferior wall MI. Lab results return with significantly elevated levels of cardiac enzymes: Troponin I is at 3.2 ng/mL (normal value <0.04 ng/mL) and CK-MB level is 56 ng/mL (normal value <5 ng/mL). This confirms the diagnosis of an acute MI. His blood glucose level is also noted to be high at 250 mg/dL, indicating poor control of his diabetes. The patient's lipid panel is also abnormal with total cholesterol at 240 mg/dL, HDL 32 mg/dL, LDL 160 mg/dL, and triglycerides 220 mg/dL, indicating dyslipidemia.

Change in Patient Status:

Shortly after the lab results come back, the patient's condition worsens. His blood pressure drops to 90/60 mmHg, his heart rate increases to 130 bpm, and his oxygen saturation falls to 85% on room air. He is increasingly short of breath and appears pale and diaphoretic. These signs suggest the patient may be developing cardiogenic shock, a serious complication of MI where reduced heart function leads to inadequate perfusion of tissues. This situation requires immediate intervention to stabilize the patient and restore perfusion. This may include medications to increase blood pressure and contractility, and possibly consideration for intra-aortic balloon pump therapy or other mechanical circulatory support.

Section 2

New Complications:

Unfortunately, the patient's condition continues to deteriorate. His oxygen saturation drops further to 80% even on 2 liters of supplemental oxygen. His heart rate escalates to 140 bpm and blood pressure drops further to 85/50 mmHg. He also begins to complain of severe, radiating chest pain that is not relieved by nitroglycerin. The patient's worsening hypoxia, tachycardia, hypotension, and unrelieved chest pain could indicate a possible extension of the myocardial infarction or impending cardiac arrest.

Additionally, patient's urine output falls to less than 20 mL/hr for the past 3 hours, suggesting decreased renal perfusion due to cardiogenic shock. His blood glucose level also rises to 300 mg/dL, indicating stress hyperglycemia. This further complicates the situation, as uncontrolled hyperglycemia can contribute to increased myocardial damage and poor outcomes in acute MI.

These new complications indicate the need for aggressive interventions to restore myocardial perfusion and manage the patient's diabetes. It may also be necessary to involve a multidisciplinary team including cardiology, endocrinology, and critical care specialists to manage his complex needs. The patient's family should also be updated about his worsening condition and potential need for more aggressive interventions.

Section 3

New Diagnostic Results:

The patient's EKG now shows ST segment elevation in multiple leads, indicating that the myocardial infarction has likely extended. Troponin levels, a marker of heart muscle damage, have also risen to 5.0 ng/mL, far above the normal limit of 0.04 ng/mL. This confirms the suspicion of an extensive myocardial infarction. Additionally, arterial blood gas (ABG) reveals a pH of 7.30, a PaCO2 of 35 mmHg, and a PaO2 of 60 mmHg, which suggests the patient is in a state of metabolic acidosis, likely secondary to lactic acidosis from poor tissue perfusion.

Furthermore, a repeat chest x-ray shows new onset pulmonary edema, a likely complication of the decreased heart function and increasing left ventricular failure. The patient's BNP (B-type natriuretic peptide), a heart failure marker, has also increased to 900 pg/mL, significantly above the normal range of up to 100 pg/mL.

These new findings necessitate immediate medical intervention. The ongoing signs of cardiogenic shock, increased markers of myocardial damage, and new evidence of heart failure and metabolic acidosis indicate a rapidly worsening situation. The healthcare team needs to reassess the treatment plan and possibly consider more aggressive treatment options such as emergency revascularization procedures or inotropic support. The patient's diabetes and renal function should also be closely monitored and managed to prevent further complications.

Section 4

Change in Patient Status:

Despite the aggressive medical intervention, the patient's condition continues to deteriorate. He becomes increasingly hypotensive, with a blood pressure now measured at 85/50 mmHg, a decrease from the initial measurement of 110/70 mmHg. His heart rate has climbed to 125 bpm from the previous 100 bpm, suggesting compensatory tachycardia. His respiratory rate has also increased to 28 breaths per minute and he appears visibly dyspneic. On auscultation, there are new crackles in both lower lung fields, indicating worsening pulmonary edema.

The patient's level of consciousness has also decreased; he is now only responsive to painful stimuli and his Glasgow Coma Scale score has dropped to 9 from 15. This could signify inadequate cerebral perfusion due to the decreased cardiac output. His skin is cold and clammy to touch, and capillary refill time is delayed to 4 seconds, further indicating poor peripheral perfusion.

These findings suggest that the patient's cardiogenic shock is rapidly progressing, and his heart is failing to adequately supply blood to his vital organs. The healthcare team needs to reassess the current management plan, as it appears to be insufficient. More advanced interventions such as mechanical circulatory support may need to be considered at this point. Concurrently, the team should continue monitoring for potential complications such as arrhythmias, acute kidney injury, or cardiopulmonary arrest.

Section 5

New Diagnostic Results:

The patient's lab results have returned, revealing an elevated troponin level of 4.5 ng/mL, significantly higher than the normal range of 0.00-0.04 ng/mL, which confirms the initial suspicion of an acute myocardial infarction. His blood urea nitrogen and creatinine levels are also elevated at 30 mg/dL and 2.2 mg/dL respectively, suggesting possible acute kidney injury secondary to decreased renal perfusion. Additionally, his arterial blood gas (ABG) shows a pH of 7.28, a PaCO2 of 50 mmHg, and a PaO2 of 65 mmHg, indicating acute respiratory acidosis and hypoxemia.

His electrocardiogram (ECG) has also shown new changes, with ST segment elevations in leads II, III, and aVF, suggestive of an inferolateral myocardial infarction. An echocardiogram reveals decreased left ventricular ejection fraction of 35%, confirming significant cardiac dysfunction.

These new results indicate further deterioration of the patient’s condition. The healthcare team now needs to consider the implications of these findings in adjusting the management plan. They will need to address his deteriorating renal function, worsening acid-base imbalance, and the extent of myocardial injury as reflected in his ECG and echocardiogram. This may involve initiating renal replacement therapy, optimizing mechanical ventilation, and considering revascularization options.