Chronic stable angina - Nursing Case Study

Pathophysiology

• Primary mechanism: Chronic stable angina primarily results from narrowing of coronary arteries due to atherosclerosis. This limits the blood flow to the heart muscle, especially during increased demand such as physical activity, causing transient ischemia (insufficient oxygen) to the heart muscle.

• Secondary mechanism: Reduced oxygen supply triggers anaerobic metabolism in heart cells, leading to accumulation of lactic acid and other metabolites. These metabolites irritate nerve endings, resulting in chest pain or discomfort, the main symptom of angina.

• Key complication: Continuous ischemia can lead to myocardial infarction (heart attack). The severity depends on the extent and duration of blocked blood flow. If not managed, this can cause irreversible damage to the heart muscle and potentially fatal arrhythmias.

Patient Profile

Demographics:

67-year-old male, retired construction worker

History:

• Key past medical history: Diagnosed with Chronic stable angina 5 years ago, Type 2 Diabetes Mellitus, hypertension, history of smoking

• Current medications: Nitroglycerin, Metformin, Lisinopril

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Persistent chest pain on exertion, feeling more fatigued than usual

• Key symptoms: Chest pain radiating to the left arm, shortness of breath, fatigue, increased frequency of angina attacks

• Vital signs: Blood pressure 160/95 mmHg, Heart rate 98 bpm, Respiratory rate 18 breaths per minute, Temperature 98.6F, Oxygen saturation 92% on room air.

Section 1

Change in Patient Status:

The patient's condition started to deteriorate rapidly. He suddenly complained of severe chest pain that was significantly worse than his usual angina. The pain was described as a crushing sensation, and he became pale, diaphoretic, and increasingly dyspneic. His oxygen saturation dropped to 88% on room air. His heart rate increased to 110 bpm and blood pressure dropped to 140/85 mmHg, indicative of his body's response to the pain and potential decreased cardiac output.

The nurse promptly placed the patient on 2 liters of oxygen via nasal cannula, which improved his oxygen saturation to 94%. However, the pain did not alleviate even after taking sublingual nitroglycerin, which usually manages his stable angina. The sudden intensifying chest pain, unresponsive to nitroglycerin, along with the changes in vital signs and oxygen requirement suggested a possible progression from chronic stable angina to acute coronary syndrome, potentially a myocardial infarction. The nurse immediately alerted the healthcare team to reassess the patient and consider further diagnostic testing.

Section 2

New Diagnostic Results:

Upon receiving the nurse's alert, the healthcare team quickly ordered an electrocardiogram (EKG) and blood work to assess the patient's cardiac markers. The EKG showed ST-segment elevations in leads II, III, and aVF, indicating an inferior wall myocardial infarction. This finding was consistent with the patient's worsening symptoms and unresponsiveness to nitroglycerin.

The patient's blood work revealed elevated troponin levels, further confirming the diagnosis of a myocardial infarction. His troponin levels were 0.5 ng/mL, significantly higher than the normal range of 0 to 0.04 ng/mL. His complete blood count (CBC) showed a slightly elevated white blood cell count at 12,000/µL, suggesting the body's response to the acute cardiac event. The rest of the CBC was within normal limits. These diagnostic findings necessitated urgent medical intervention to restore blood flow to the affected heart muscle and prevent further damage. The team decided to activate the hospital's cardiac catheterization lab for an emergent percutaneous coronary intervention.

Section 3

Change in Patient Status and New Complications:

Unfortunately, while preparing for the emergent coronary intervention, the patient's condition started to decline. His blood pressure dropped to 90/60 mm Hg, and his heart rate increased to 110 beats per minute, indicating signs of cardiogenic shock. The patient also began to complain of increased chest pain, now rating it as a 9 on a scale of 1-10, and became diaphoretic and increasingly anxious.

At the same time, the patient's latest blood work showed a rising troponin level of 1.0 ng/mL, and his EKG now revealed the development of Q waves in leads II, III, and aVF, suggestive of an evolving myocardial infarction. This deterioration in the patient's status necessitated immediate action. The healthcare team decided to administer intravenous fluids and started the patient on an intravenous nitroglycerin drip to help stabilize his hemodynamic status while continuing to expedite the process for his transfer to the cardiac catheterization lab.

Section 4

Despite the initiation of intravenous fluids and nitroglycerin, the patient's blood pressure remained unstable, fluctuating between 80/50 mm Hg and 90/60 mm Hg, while his heart rate remained tachycardic at 120 beats per minute. The patient also reported persistent chest pain, rating it now as a 10 on a scale of 1-10, despite the administration of nitroglycerin. Additionally, his oxygen saturation level began to dip, falling to 88% on room air, indicating possible oxygen deprivation to his tissues.

In response to these findings, the healthcare team ordered a repeat EKG and a chest X-ray. The new EKG showed increased Q wave depth in leads II, III, and aVF, confirming the presence of myocardial infarction. The chest X-ray revealed pulmonary edema, suggestive of congestive heart failure, a common complication of untreated myocardial infarction. Further blood work showed a further increase in troponin levels to 2.1 ng/mL, indicative of ongoing cardiac damage. These findings required an immediate change in the care plan, necessitating urgent revascularization to salvage the infarcted myocardium and prevent further complications. As the team prepared for the cath lab, the patient was started on supplemental oxygen to address his hypoxia.

Section 5

Upon arrival at the cath lab, the patient's blood pressure had further decreased to 75/40 mm Hg. He became increasingly agitated, reporting increased chest discomfort and increasing shortness of breath, despite being on supplemental oxygen. His oxygen saturation levels had also further decreased to 85%, demonstrating that the patient's tissue oxygenation was still inadequate. The healthcare team promptly intubated and ventilated the patient, ensuring an adequate oxygen supply to his vital organs.

The coronary angiogram showed severe triple vessel disease with a total occlusion in the right coronary artery. This finding was consistent with the EKG changes observed earlier and explained the patient's persistently unstable condition. The cardiologist decided to perform an emergency coronary artery bypass graft (CABG) surgery, considering the extent of the disease and the patient's deteriorating condition.

The new complications added another layer of complexity in managing this patient. The nursing team needed to closely monitor the patient's vital signs, manage his pain, and ensure adequate oxygenation before, during, and after the surgery. The team also had to prepare for post-operative care, considering the patient's risk for complications such as arrhythmias, myocardial reinfarction, and low cardiac output syndrome. This case highlighted the importance of swift clinical reasoning, timely interventions, and multidisciplinary teamwork in managing patients with complex and critical conditions.