myocardial infarciton - Nursing Case Study
Pathophysiology
• Primary mechanism: Plaque rupture - Atherosclerotic plaque within coronary arteries ruptures, causing blood clot formation at the site. This obstructs blood flow to a section of the heart, depriving it of oxygen and nutrients, leading to myocardial necrosis or heart tissue death.
• Secondary mechanism: Supply-demand mismatch - In certain conditions such as severe anemia or tachyarrhythmias, the oxygen demand of the heart exceeds the supply, even without plaque rupture. This can also lead to myocardial infarction.
• Key complication: Ventricular arrhythmias - Lost/damaged heart tissue disrupts electrical pathways, causing irregular heart rhythms. Ventricular arrhythmias, like ventricular fibrillation, can be life-threatening, leading to cardiac arrest if not treated immediately.
Patient Profile
Demographics:
64-year-old male, retired construction worker
History:
• Key past medical history: Hypertension, Type 2 Diabetes, High cholesterol
• Current medications: Metformin, Atorvastatin, Lisinopril
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Sudden severe chest pain radiating to the left arm, shortness of breath
• Key symptoms: Sweating, lightheadedness, nausea, and vomiting
• Vital signs: Blood pressure 160/90 mmHg, Heart rate 110 beats per minute, Respiratory rate 24 breaths per minute, Temperature 98.6°F, Oxygen saturation 92% on room air.
Section 1
New Diagnostic Results:
The patient was immediately taken to the catheterization lab for a coronary angiography, which revealed a 90% occlusion in the left anterior descending artery (LAD). At this point, the decision was made to perform a percutaneous coronary intervention (PCI). The procedure was successful in reestablishing blood flow, however, post-PCI troponin levels significantly elevated at 2.3 ng/mL, significantly higher than the normal range of 0.00-0.04 ng/mL, indicating significant myocardial damage.
Change in Patient Status:
Post-PCI, the patient's chest pain eased considerably. However, he now reported feeling fatigued, with continued shortness of breath. His oxygen saturation dropped to 88% on room air, and his respiratory rate increased to 28 breaths per minute. His blood pressure also dropped to 130/80 mmHg, with a heart rate of 90 beats per minute. EKG showed ST segment depression indicating potential myocardial ischemia. The patient was started on supplemental oxygen and was closely monitored for signs of heart failure or other complications.
These changes in the patient's status suggest possible complications post-PCI, such as reperfusion injury, or possibly the onset of heart failure due to the myocardial damage caused by the initial infarction. This requires further investigation and monitoring to confirm and manage these potential complications.
Section 2
New Complications:
Over the next few hours, the patient's condition began to deteriorate further. His oxygen saturation dropped to 84% despite the supplemental oxygen, and his respiratory rate further increased to 32 breaths per minute. The patient also complained of increasing fatigue and a new onset of confusion, which may be indicative of hypoxia. He developed a productive cough, with frothy pink sputum, suggesting the possibility of acute pulmonary edema, a common complication of heart failure. His blood pressure continued to drop, now registering at 120/70 mmHg with a heart rate of 100 beats per minute.
Response to Interventions:
In response to these new complications, the medical team decided to increase the patient's oxygen supply and initiated non-invasive positive pressure ventilation (NIPPV) to help improve his oxygenation. They also administered intravenous diuretics to help alleviate the pulmonary edema. An arterial blood gas was ordered, which showed a PaO2 of 60 mmHg, PaCO2 of 35 mmHg, and a pH of 7.35, suggesting acute respiratory distress syndrome (ARDS). A chest X-ray was also ordered to confirm the suspected pulmonary edema.
The patient's clinical deterioration post-PCI and the new onset of pulmonary edema and possible ARDS underscore the complexity of managing myocardial infarction, especially in patients with significant myocardial damage. The patient's condition requires vigilant monitoring, prompt interventions, and a multidisciplinary approach to care.
Section 3
New Diagnostic Results:
The chest X-ray confirmed the presence of acute pulmonary edema, with bilateral infiltrates noted. The EKG showed persistent ST-segment elevations, suggesting ongoing myocardial injury. Meanwhile, the patient's lab results returned, showing a significant increase in troponin levels from 2.0 ng/mL to 6.8 ng/mL, indicative of further myocardial damage. The B-type natriuretic peptide (BNP) level was also notably elevated at 900 pg/mL, which is consistent with the diagnosis of heart failure.
Change in Patient Status:
Despite the interventions, the patient's oxygen saturation continued to fluctuate between 84% and 88%. His respiratory rate remained high, and his breath sounds were noted to be crackles bilaterally, suggestive of continued pulmonary edema. The patient's blood pressure dropped further to 100/60 mmHg, and his heart rate increased to 110 beats per minute. He became increasingly lethargic and less responsive to verbal stimulation. His skin was cool and clammy, and his extremities were noted to be cyanotic. These changes in the patient's condition indicate a worsening of his heart failure and potential cardiogenic shock, requiring immediate further intervention.
Section 4
New Complications:
Late in the evening, the patient's condition declined rapidly. He began showing signs of altered mental status, becoming increasingly confused and disoriented, and complained of severe chest pain that radiated to his left arm. His oxygen saturation dropped further to 80%, despite supplemental oxygen. His blood pressure plummeted to 90/50 mmHg, and his heart rate spiked to 130 beats per minute. On auscultation, his breath sounds were muffled, and his heart sounds were distant. The EKG showed new-onset, wide QRS complexes, suggestive of ventricular tachycardia, which is a life-threatening rhythm.
In addition, the patient's lab results returned showing a further increase in his troponin levels to 10.0 ng/mL, confirming the progression of myocardial damage. His BNP level also increased to 1200 pg/mL, demonstrating worsening heart failure. The patient's deteriorating condition is indicative of severe heart failure with cardiogenic shock and the onset of life-threatening arrhythmia. This situation requires a high level of clinical reasoning, as the patient will need immediate aggressive interventions to prevent further cardiac damage and stabilize his condition. This could potentially involve medication administration, electrical cardioversion, and even emergency surgery.
Section 5
Change in Patient Status:
Despite aggressive interventions, the patient's condition continued to deteriorate. His oxygen saturation dropped to 75%, and his blood pressure fell further to 85/45 mmHg. His heart rate continued to race at 140 beats per minute, and he became non-responsive to verbal stimuli. His skin became cool, clammy and pale, and his pulse was weak and thready. He was also observed to have irregular, shallow breathing and his peripheral pulses were not palpable.
Response to Interventions:
The Rapid Response Team was immediately called and advanced cardiac life support (ACLS) protocol was initiated. The patient was intubated and mechanical ventilation started to support his respiratory failure. Intravenous vasopressors, including dopamine and norepinephrine, were administered to increase his blood pressure and heart rate. Despite these efforts, the patient's EKG continued to show ventricular tachycardia. The team decided to proceed with synchronized cardioversion, which was temporarily successful in restoring a normal heart rhythm. However, the patient remained hemodynamically unstable, demanding further intensive care and monitoring. His worsening condition has opened up a new set of complications that may require even more invasive interventions like intra-aortic balloon pump (IABP) or ventricular assist device (VAD).