Chronic stable angina - Nursing Case Study
Pathophysiology
• Primary mechanism: Chronic stable angina arises from reduced blood flow to the heart muscle due to the partial blockage of coronary arteries. This blockage is typically the result of atherosclerosis, where plaque comprising fat, cholesterol, and other substances accumulate and harden on the artery walls, narrowing the artery lumen and limiting blood flow.
• Secondary mechanism: In response to reduced blood flow, the heart muscle demands more oxygen during physical exertion or stress, causing chest pain or discomfort known as angina. The pain usually subsides with rest when oxygen demand decreases.
• Key complication: With time, the continued restriction of blood flow can cause ischemic heart disease, potentially leading to serious complications like heart attack or arrhythmias due to prolonged oxygen deprivation to the heart muscle.
Patient Profile
Demographics:
60 years old, Male, Retired construction worker
History:
• Key past medical history: Hypertension, Type 2 diabetes, smoker for 40 years
• Current medications: Metformin, Lisinopril, Nicotine patches
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Persistent chest pain especially during physical activities
• Key symptoms: Shortness of breath, fatigue, nausea, excessive sweating, pain radiating to left arm
• Vital signs: Blood pressure 155/95 mmHg, pulse 85 bpm, temperature 98.6°F, respiratory rate 20 breaths/minute
Section 1
Change in Patient Status:
Over the next couple of days, the patient's chest pain becomes increasingly frequent, even at rest. He reports a pain level of 8 on a scale of 10, and further describes the pain as a crushing sensation. His shortness of breath worsens, and he experiences dizziness and confusion. His vital signs now read: Blood pressure 170/100 mmHg, pulse 90 bpm, temperature 98.7°F, respiratory rate 24 breaths/minute.
These symptoms suggest that the patient's chronic stable angina may be progressing to unstable angina, a more severe form of coronary artery disease where symptoms occur more frequently and without any triggering factors, even during rest. The increased frequency and intensity of chest pain, elevated blood pressure, and increasing pulse rate suggest that the patient's heart is working harder to compensate for the reduced blood flow. The dizziness and confusion may be signs of hypoxia as the heart struggles to meet the body's oxygen demand. The patient's history of hypertension, diabetes, and smoking further increase his risk for unstable angina and potential myocardial infarction. Prompt reassessment and intervention are necessary to prevent further complications.
Section 2
New Diagnostic Results:
Upon further evaluation, an electrocardiogram (ECG) was performed which showed ST-segment depression and T-wave inversion, indicative of myocardial ischemia. His troponin levels were also checked, which came back slightly elevated at 0.06 ng/mL, further suggesting cardiac damage. Additionally, a lipid panel showed increased levels of total cholesterol (250 mg/dL), LDL cholesterol (160 mg/dL), and triglycerides (200 mg/dL), with decreased levels of HDL cholesterol (35 mg/dL).
These new diagnostic results corroborate the suspicion of progressing unstable angina. The ECG changes are suggestive of ongoing cardiac ischemia and coupled with the elevated troponin levels, indicate that the patient might already be having a non-ST elevation myocardial infarction (NSTEMI). The abnormal lipid profile further underlines the patient's increased risk for coronary artery disease. The healthcare team needs to apply clinical reasoning to make prompt decisions on necessary interventions, including medication adjustments and possibly invasive procedures like percutaneous coronary intervention (PCI).
Section 3
Change in Patient Status:
Over the next 24 hours, the patient's condition began to deteriorate. He began to complain of more frequent chest pain, rating it as an 8 on a scale of 1 to 10. The pain, which he described as a heavy pressure in his chest, was unrelieved by his usual nitroglycerin. Additionally, he reported experiencing shortness of breath, even at rest, and feeling excessively fatigued. On physical examination, his blood pressure was 140/90 mmHg, pulse was 100 bpm, and respirations were increased to 22 breaths per minute. His oxygen saturation dropped to 92% on room air.
This change in the patient's condition signals a worsening of his cardiac status. The increased frequency and intensity of his chest pain, despite nitroglycerin, suggest that the ischemia is worsening. His shortness of breath and increased respiratory rate could indicate the development of heart failure, as the failing heart is unable to pump enough oxygenated blood to meet the body's needs. The elevated blood pressure, increased heart rate, and decreased oxygen saturation are all signs of his body's attempt to compensate for the decreased cardiac output. This deterioration necessitates swift reassessment of the patient's treatment plan and possible escalation of care.
Section 4
New Diagnostic Results:
Further diagnostic tests were performed to evaluate the patient's deteriorating condition. His EKG revealed new ST-segment depression, indicating myocardial ischemia. His cardiac biomarkers, including troponin T, were elevated, suggesting possible myocardial injury. A chest X-ray showed signs of pulmonary congestion, hinting at the possibility of heart failure. His B-type natriuretic peptide (BNP), a marker for heart failure, was also significantly elevated at 900 pg/mL (normal range: 0 -100 pg/mL).
These new findings provided a clearer picture of the patient's deteriorating cardiac status. The elevated cardiac markers, in conjunction with the EKG changes, suggested that the patient was experiencing an acute coronary syndrome, possibly unstable angina or possibly even a myocardial infarction. The signs of pulmonary congestion and elevated BNP level indicated that heart failure was also a major concern. This new information necessitated a reevaluation of the patient's treatment plan and a possible escalation of care. The nursing team would need to closely monitor the patient for further deterioration and be prepared to intervene as necessary.
Section 5
Change in Patient Status:
Over the next few hours, the patient's condition continued to deteriorate. His pulse rate increased to 120 beats per minute (normal range: 60-100 bpm) and his blood pressure fell to 90/60 mm Hg (normal range: 120-130/80-90 mm Hg), indicating possible cardiogenic shock. His breath sounds were increasingly crackly on auscultation, suggesting worsening pulmonary congestion. He complained of persistent chest pain, rating it 8 out of 10 on the pain scale. His oxygen saturation dropped to 90% on room air (normal range: 95%-100%), confirming that his respiratory status was being compromised.
The patient's worsening hemodynamic status, persistent chest pain, and decreased oxygen saturation were concerning signs of escalating cardiac dysfunction. The combined clinical picture pointed towards an acute coronary syndrome progressing towards heart failure and shock. The nursing team, recognizing the severity of the situation, activated rapid response and prepared the patient for possible transfer to the Intensive Care Unit (ICU). This change in status required immediate medical intervention and a critical reassessment of the patient's treatment plan. The team needed to work quickly, yet diligently, to prevent further cardiac damage and stabilize the patient.