nstemi - Nursing Case Study

Pathophysiology

• Primary mechanism: NSTEMI is primarily caused by the rupture of a vulnerable atherosclerotic plaque in a coronary artery, which leads to partial occlusion by a thrombus. This reduces blood flow, causing subendocardial ischemia and myocardial injury without full-thickness necrosis.

• Secondary mechanism: The resultant decrease in oxygen delivery to the cardiac tissue triggers a cascade of cellular damage, including disruption of ATP production and accumulation of metabolic waste, which exacerbates myocardial dysfunction.

• Key complication: This ischemic process can lead to severe complications such as heart failure or arrhythmias, due to impaired contractility and electrical instability of the affected myocardial tissue.

Patient Profile

Demographics:

64-year-old male, retired construction worker

History:

• Key past medical history: Hypertension, Type 2 Diabetes Mellitus, Chronic Kidney Disease Stage 3, Hyperlipidemia, Former smoker (30 pack-year history)

• Current medications: Lisinopril 20 mg daily, Metformin 1000 mg twice daily, Atorvastatin 40 mg daily, Aspirin 81 mg daily

• Allergies: Penicillin (rash)

Current Presentation:

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

• Key symptoms: Shortness of breath, diaphoresis, nausea, dizziness

• Vital signs: Blood Pressure 180/110 mmHg, Heart Rate 120 bpm, Respiratory Rate 28 breaths per minute, Temperature 37.8°C, Oxygen Saturation 89% on room air

Section 1

New Diagnostic Results:

Following the initial assessment, the medical team decided to conduct a series of urgent diagnostic tests to evaluate the extent of myocardial injury and assess the patient's overall condition. The 12-lead ECG revealed ST-segment depression in leads II, III, aVF, and V4-V6, consistent with subendocardial ischemia. Troponin I levels were markedly elevated at 4.5 ng/mL, indicating significant myocardial injury. An echocardiogram was performed, showing moderately reduced left ventricular ejection fraction at 40%, suggesting impaired cardiac contractility. The presence of regional wall motion abnormalities in the inferolateral segments confirmed the impact of the ischemic process.

Additional laboratory tests highlighted further complications. Serum creatinine was elevated at 2.5 mg/dL, indicating worsening renal function, likely exacerbated by the acute cardiac event and poor renal perfusion. Blood glucose levels were uncontrolled at 256 mg/dL, reflecting the impact of stress hyperglycemia on his diabetic status. Lipid panel results revealed LDL levels of 145 mg/dL, underscoring persistent hyperlipidemia despite ongoing statin therapy. Chest X-ray findings suggested mild pulmonary congestion, raising concerns about emerging heart failure.

These diagnostic outcomes prompted the healthcare team to intensify the treatment plan, focusing on stabilizing the patient's hemodynamics and addressing the multi-system complications. Given the patient's complex medical history and current instability, advanced critical thinking and coordinated care across cardiology, nephrology, and endocrinology specialties are essential to optimize outcomes and prevent further deterioration. The team is also planning a coronary angiography to assess the need for potential revascularization, while carefully monitoring for signs of acute heart failure or arrhythmias.

Section 2

Change in Patient Status:

As the medical team closely monitored the patient, several changes in clinical status emerged, necessitating immediate attention and adjustment of the treatment strategy. Approximately 12 hours post-admission, the patient began to exhibit signs of acute decompensation. His blood pressure dropped to 88/54 mmHg, indicating potential cardiogenic shock. Heart rate increased to 110 beats per minute, and the patient complained of increased dyspnea, now requiring supplemental oxygen via a non-rebreather mask to maintain an oxygen saturation of 92%. Auscultation of the lungs revealed bilateral crackles, suggesting a progression in pulmonary congestion likely due to worsening heart failure.

Laboratory tests revealed a further decline in renal function with serum creatinine rising to 3.0 mg/dL, exacerbating concerns about the patient’s ability to tolerate standard heart failure treatments. Additionally, arterial blood gas analysis showed a pH of 7.32, pCO2 of 48 mmHg, and HCO3- of 20 mmol/L, indicating a mixed respiratory and metabolic acidosis. Despite insulin adjustments, blood glucose levels remained elevated at 280 mg/dL, complicating the management of the patient's diabetes amidst the acute stress response.

In light of these developments, the interdisciplinary team convened to reassess and optimize the management plan. Pharmacologic support was intensified, with cautious initiation of inotropic agents to stabilize hemodynamics while considering the risks of further renal compromise. Diuretic therapy was adjusted carefully to manage fluid overload without inducing renal hypoperfusion. The patient's deteriorating condition highlighted the need for advanced critical care interventions, including potential consideration for mechanical circulatory support if hemodynamics failed to stabilize. This critical juncture demanded vigilant monitoring for arrhythmias and ongoing collaboration among cardiology, nephrology, and intensive care teams to navigate the complex interplay of organ systems and optimize patient outcomes.

Section 3

New Complications

Despite the intensified management efforts, the patient began to develop new complications that further complicated the clinical picture. Approximately 18 hours post-admission, the patient's rhythm strip indicated episodes of ventricular tachycardia, raising the concern for potential electrical instability secondary to ischemia and electrolyte imbalances. The interdisciplinary team swiftly initiated antiarrhythmic therapy, carefully balancing the need to control the arrhythmia with the risk of exacerbating the patient's already tenuous hemodynamic status. Continuous cardiac monitoring was prioritized to detect any further arrhythmic events promptly.

Concurrently, a repeat set of laboratory tests showed a significant drop in hemoglobin levels to 9.8 g/dL, suggesting possible gastrointestinal bleeding, likely exacerbated by antiplatelet and anticoagulant therapy initiated for NSTEMI management. The patient reported new-onset melena, which was confirmed upon examination. This development necessitated an urgent gastroenterology consult for evaluation and potential intervention to address the bleeding source. The team faced the complex challenge of balancing bleeding risk with thrombotic risk, requiring meticulous adjustment of anticoagulation therapy under the guidance of both cardiology and gastroenterology.

As the patient's condition continued to evolve, the medical team also observed signs of progressive right-sided heart failure, indicated by rising jugular venous pressure and worsening peripheral edema. This was compounded by the patient's persistent pulmonary congestion despite ongoing diuretic therapy, suggesting an inadequate response to current heart failure management strategies. In light of these complications, the team considered the necessity of advanced hemodynamic monitoring and potential escalation to mechanical circulatory support, such as an intra-aortic balloon pump, to provide temporary stabilization and allow time for diagnostic and therapeutic interventions to address the multifaceted challenges at hand. This critical phase of the patient's journey demanded an integrated approach, leveraging the expertise of multiple specialties to navigate the complex interdependencies of the patient's condition and optimize outcomes.

Section 4

New Diagnostic Results

The interdisciplinary team's decision to implement advanced hemodynamic monitoring provided crucial insights into the patient's increasingly precarious status. A right heart catheterization was performed to elucidate the underlying hemodynamic derangements. The results revealed a significantly elevated right atrial pressure of 15 mmHg and a pulmonary artery pressure of 45/25 mmHg, confirming right-sided heart failure. The cardiac index was calculated at 1.8 L/min/m², indicating severe cardiac output compromise. These findings underscored the urgent need to reassess and potentially escalate heart failure management strategies, including consideration for inotropic support and mechanical assist devices.

Simultaneously, the gastroenterology team proceeded with an urgent endoscopy, which identified multiple gastric ulcers with a visible vessel in one of the lesions, indicating a high risk for rebleeding. Hemostasis was achieved through endoscopic intervention, but the team remained vigilant due to the ongoing requirement for antiplatelet and anticoagulant therapy. To mitigate the bleeding risk, a delicate balance was struck with a modified anticoagulation regimen, closely monitored through serial coagulation profiles.

Further complicating the scenario, the patient began to exhibit signs of acute kidney injury, with serum creatinine rising from 1.1 mg/dL at baseline to 2.3 mg/dL. This renal impairment was attributed to a combination of factors including hypoperfusion from reduced cardiac output, diuretic use, and possible nephrotoxic effects of medications. The nephrology team was consulted to guide renal protective strategies while optimizing fluid status to prevent exacerbation of heart failure. This intricate interplay of systems required the medical team to continuously integrate evolving data, adjusting therapeutic approaches in real-time to navigate the complexities of the patient's deteriorating condition.

Section 5

New Complications

As the medical team continued to navigate the complexities of the patient's condition, a new challenge arose. During the evening shift, the patient developed acute shortness of breath and peripheral cyanosis, prompting an urgent reassessment. Upon examination, the patient's vital signs revealed a heart rate of 128 beats per minute, blood pressure of 85/50 mmHg, respiratory rate of 30 breaths per minute, and an oxygen saturation of 84% on a non-rebreather mask. Auscultation of the lungs revealed diffuse crackles, indicating pulmonary congestion. These findings suggested an acute decompensation of heart failure with possible cardiogenic shock, attributable to the severely compromised cardiac output and fluid overload.

In response to this critical change in status, the team initiated advanced interventions. The patient was intubated and placed on mechanical ventilation to support respiratory function and optimize oxygenation. Additionally, a norepinephrine infusion was started to stabilize blood pressure and augment systemic perfusion. Despite these measures, the patient continued to exhibit signs of end-organ hypoperfusion, including altered mental status and cool extremities. Laboratory results showed a worsening lactate level of 5.2 mmol/L and elevated liver enzymes, further indicating the severity of the shock state.

Recognizing the gravity of the situation, the interdisciplinary team convened to reassess the treatment plan. There was discussion regarding the potential need for an intra-aortic balloon pump or even extracorporeal membrane oxygenation (ECMO) to provide circulatory support. Meanwhile, diuretic therapy was cautiously adjusted to manage the volume status without further compromising renal function. The nephrology team recommended continuous renal replacement therapy (CRRT) to address the acute kidney injury while maintaining hemodynamic stability. This complex interplay of interventions required rigorous monitoring and swift clinical decision-making, as the team sought to stabilize the patient and prevent further deterioration.