Chronic stable angina - Nursing Case Study

Pathophysiology

• Primary mechanism: Coronary Artery Disease (CAD) - Chronic stable angina typically stems from CAD where fatty plaque build-up narrows the coronary arteries, reducing blood flow to the heart. This results in an imbalance between myocardial oxygen supply and demand, especially during physical exertion or emotional stress.

• Secondary mechanism: Oxygen supply-demand mismatch - Angina symptoms arise when the heart muscle's oxygen demand surpasses the reduced supply due to the narrowed arteries. The mismatch triggers pain signaling pathways, resulting in the characteristic chest discomfort of angina.

• Key complication: Myocardial ischemia - If the oxygen supply-demand mismatch persists, it can lead to myocardial ischemia. Chronic myocardial ischemia can cause heart muscle damage over time, potentially leading to heart failure or arrhythmias.

Patient Profile

Demographics:

62-year-old male, retired construction worker

History:

• Key past medical history: Diagnosed with hypertension and hyperlipidemia 10 years ago, history of smoking, no previous surgeries

• Current medications: Amlodipine, Atorvastatin, Aspirin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Chest pain that worsens with physical activity and reduces with rest

• Key symptoms: Shortness of breath, fatigue, pain radiating to left arm, occasional episodes of dizziness

• Vital signs: Blood pressure 160/95 mmHg, heart rate 95 bpm, respiration rate 20 breaths per minute, temperature 98.2 F, Oxygen saturation 93% on room air.

Section 1

New Diagnostic Results:

Further diagnostic tests were ordered to evaluate the extent of the patient's CAD. An electrocardiogram (EKG) was performed, which showed ST-segment depression and T-wave inversion indicating subendocardial ischemia. A stress test was also conducted, but had to be terminated early due to the patient developing severe chest pain and dyspnea. The early termination of the stress test and the EKG changes suggest significant CAD.

A subsequent coronary angiogram revealed multiple significant stenoses in the left anterior descending (LAD) and right coronary arteries (RCA). Laboratory results also showed elevated total cholesterol levels at 240 mg/dL (normal <200 mg/dL) and LDL cholesterol at 160 mg/dL (normal <100 mg/dL), further supporting the diagnosis of hyperlipidemia.

These findings indicate the need for more aggressive management of the patient's CAD and hyperlipidemia. The severe stenoses observed may necessitate revascularization procedures, such as percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG), to restore adequate blood flow to the heart muscle. Additionally, the patient's elevated cholesterol levels suggest that current atorvastatin dosage may not be sufficient, requiring a re-evaluation of his lipid-lowering therapy. The patient's smoking history also needs to be addressed as it significantly contributes to his CAD and overall cardiovascular risk.

Section 2

Change in Patient Status:

Over the next few days, the patient's condition worsened. He started complaining of increased chest pain, even at rest, and he was visibly short of breath with minimal exertion. His blood pressure was noted to fluctuate, with readings varying from 140/90 mmHg to 160/100 mmHg, and his heart rate was persistently elevated at 110-120 beats per minute. His oxygen saturation also dropped to 92% on room air, from a previous 98%.

Initial Assessment Findings:

On further assessment, the patient appeared anxious and was sweating profusely. Cardiac auscultation revealed a regular rhythm but the heart rate was tachycardic. He had also gained 2 pounds since his last weight check 2 days ago, raising concerns for possible fluid retention. His electrocardiogram (EKG) now showed new ST-segment elevation in the anterior leads, indicating a possible progression from stable angina to an acute coronary syndrome (ACS), potentially an ST-segment elevation myocardial infarction (STEMI).

The worsening symptoms, vital sign changes, and weight gain indicated a potential acute coronary event and decompensated heart failure. This necessitated immediate medical intervention and re-evaluation of his treatment plan. The possibility of a more invasive procedure like PCI or CABG may need to be considered. It also suggested the need for more aggressive blood pressure control and potentially starting the patient on diuretic therapy for his possible fluid retention.

Section 3

New Diagnostic Results:

Following the initial assessment, further diagnostic tests were ordered to better understand the patient's worsening condition. His troponin levels were found to be significantly elevated at 2.5 ng/mL, indicative of myocardial damage. His B-type natriuretic peptide (BNP) levels were also markedly raised at 900 pg/mL, suggesting the presence of heart failure. In addition, his blood tests showed a mild increase in creatinine levels from 0.9 mg/dL to 1.3 mg/dL, hinting at possible renal insufficiency, likely secondary to his deteriorating cardiac status.

A repeat echocardiogram revealed a decreased ejection fraction (EF) of 40%, compared to his previous EF of 55%, confirming the suspicion of heart failure. Interestingly, the echocardiogram also showed new regional wall motion abnormalities in the anterior wall, consistent with the EKG findings of anterior ST-segment elevation.

These new diagnostic results support the initial assessment findings and suggest a progression of the patient's condition from stable angina to acute coronary syndrome with concomitant heart failure. The rising creatinine levels also indicate that the patient's kidneys may be affected by his worsening cardiac status. This raises the need for careful consideration of the patient's fluid and medication management, given the potential for renal impairment. The complexity of the patient's condition necessitates a multidisciplinary approach, involving cardiologists, nephrologists, and critical care specialists.

Section 4

Change in Patient Status:

Over the next 24 hours, the patient's condition continued to deteriorate. He developed increasing shortness of breath, even at rest, accompanied by a persistent, dry cough. His blood pressure also became unstable, fluctuating between 160/90 mmHg and 100/60 mmHg. His pulse rate increased to 105 beats per minute, likely compensatory in response to his deteriorating cardiac function. His oxygen saturation dropped to 90% on room air, necessitating supplemental oxygen.

New Complications:

In addition to his worsening cardiac status, the patient also developed oliguria. His urine output decreased to less than 30 mL/hour over a period of six hours, suggesting worsening renal function. His serum creatinine levels increased further to 1.6 mg/dL, and blood urea nitrogen (BUN) rose to 28 mg/dL, indicative of acute kidney injury (AKI). The combination of his deteriorating cardiac status, unstable BP, and declining renal function suggests the development of cardiorenal syndrome. This complicates the management of his fluid status, as aggressive fluid resuscitation to treat his heart failure could exacerbate his AKI. Similarly, diuretic use to manage his fluid overload might further impair his renal function. This complex clinical scenario requires careful balancing of both cardiac and renal considerations in his treatment plan.

Section 5

New Diagnostic Results:

The patient's worsening condition prompted additional diagnostic tests. An echocardiogram revealed a decrease in the left ventricular ejection fraction (LVEF) to 35%, confirming a decline in cardiac function. Serum levels of the cardiac biomarkers—troponin I and B-natriuretic peptide (BNP)—were also elevated at 0.6 ng/mL and 900 pg/mL, respectively, indicating ongoing cardiac damage and increased cardiac strain. A repeat chest X-ray showed increased pulmonary congestion, further suggesting heart failure.

On the renal side, urinary electrolytes revealed a fractional excretion of sodium (FeNa) of 2.5%, higher than the normal range of under 1%. This was suggestive of an intrinsic renal injury. A renal ultrasound showed increased echogenicity and decreased corticomedullary differentiation, suggesting an acute tubular necrosis as a probable cause of the AKI.

This new information suggests that the patient is dealing with acute decompensated heart failure and AKI, likely secondary to decreased renal perfusion from the worsening cardiac status. This makes the management of the patient more challenging as the treatment of one condition could potentially worsen the other. The nursing team must now utilize this information to devise a comprehensive plan of care that addresses both the heart failure and the AKI.