CAD - Nursing Case Study

Pathophysiology

• Primary mechanism: Atherosclerosis - CAD develops when the coronary arteries, which supply blood to the heart muscle, become hardened and narrowed due to the buildup of plaque, a substance made up of cholesterol and other cellular waste products. This inhibits oxygen-rich blood from reaching the myocardium, causing ischemia and potentially leading to angina or heart attacks.

• Secondary mechanism: Endothelial Dysfunction - Continuous exposure to risk factors such as hypertension, smoking, diabetes, and hyperlipidemia can damage the endothelial lining of the coronary arteries. This leads to diminished production or availability of nitric oxide, a molecule that helps maintain arterial dilation and prevents platelet aggregation or thrombosis, exacerbating atherosclerosis.

• Key complication: Myocardial Infarction - If a plaque ruptures, it can cause a blood clot to form on its surface. If the clot becomes large enough, it can partially or completely block blood flow through the coronary

Patient Profile

Demographics:

57 years old, male, construction worker

History:

• Key past medical history: Hypertension, high cholesterol, diabetes type 2

• Current medications: Atenolol, Lipitor, Metformin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Chest pain and shortness of breath

• Key symptoms: Persistent chest pain, fatigue, dizziness, palpitations

• Vital signs: Blood pressure 160/100 mmHg, heart rate 100 bpm, respiratory rate 22 breaths per minute, temperature 37.2 C, oxygen saturation 93% on room air.

Section 1

Change in patient status:

The patient's condition deteriorated overnight. He was restless, with increased shortness of breath and pronounced sweating. The telemetry monitor showed frequent episodes of ventricular tachycardia. His pain seemed to be uncontrolled, rated 8/10, despite receiving scheduled doses of pain medication. His vital signs were unstable with blood pressure dropping to 130/90 mmHg, heart rate rising to 120 bpm, respiratory rate increasing to 28 breaths per minute, and oxygen saturation falling to 88% on 2 liters of nasal cannula oxygen. His skin was cool and clammy, and he looked visibly frightened.

Additional diagnostic tests were ordered, and the results showed elevated Troponin levels at 0.5 ng/mL (normal range <0.04 ng/mL), indicative of myocardial injury. An EKG revealed ST-segment elevation, suggestive of an acute myocardial infarction. The patient's blood glucose levels were also elevated at 250 mg/dL, likely due to the stress response. The nurse alerted the healthcare team about the deteriorating status and the need for urgent intervention.

Section 2

New complications:

As the day progressed, the patient's condition continued to show signs of deterioration. His blood pressure further dropped to 110/80 mmHg, and his heart rate elevated to 130 bpm. His respiratory rate also increased to 30 breaths per minute, and oxygen saturation further fell to 84% despite increasing the supplemental oxygen to 3 liters. The patient's level of consciousness also began to decrease, as evidenced by a Glasgow Coma Scale score of 13/15. He was less responsive to verbal stimuli and his speech was slurred.

The nurse also noted a new onset of irregular heart rhythm on the telemetry monitor, suggestive of atrial fibrillation. A follow-up blood test showed that the patient's Troponin levels had further increased to 0.8 ng/mL, indicating ongoing cardiac injury. The patient's creatinine levels were also elevated at 2.5 mg/dL (normal range 0.6-1.2 mg/dL), suggesting possible acute kidney injury likely due to decreased cardiac output. The healthcare team was duly informed about these new developments and the need for further urgent intervention. This situation called for heightened clinical reasoning, including re-evaluation of the current treatment plan, consideration of possible causes of the new complications, and potential new interventions to manage these complications.

Section 3

Further evaluation of the patient's condition revealed worsening symptoms. The patient complained of increased chest pain, rated 8/10 on the pain scale, associated with shortness of breath. On physical examination, the nurse observed the patient's skin was pale, cool, and clammy. On auscultation, crackles were heard over the lung bases, suggestive of fluid accumulation due to possible heart failure. The nurse also noted the patient's urine output had significantly decreased to less than 30 mL per hour over the past few hours, further indicating reduced kidney function.

A 12-lead ECG was performed which confirmed the presence of atrial fibrillation. The ECG also showed new ST-segment elevations in inferior leads, suggestive of an ongoing inferior wall myocardial infarction. Subsequently, an echocardiogram revealed a reduced ejection fraction of 35% (normal range 55-70%), indicating decreased cardiac output. These findings necessitated immediate revision of the patient's management plan and prompted the healthcare team to consider more aggressive interventions. The nurse prepared the patient for possible emergency cardiac catheterization and ensured that all necessary protocols were in place to manage the evolving situation.

Section 4

Following the cardiac catheterization, the patient's condition seemed to deteriorate further. The patient's heart rhythm was becoming more irregular, with frequent episodes of ventricular tachycardia. The patient's blood pressure dropped to 90/60 mmHg and the pulse was weak and irregular at 130 beats per minute. The patient complained of increasing shortness of breath, and the nurse noted an increase in the patient's respiratory rate to 30 breaths per minute, with shallow respiration. Oxygen saturation fell to 88% on room air, indicating severe hypoxia. The patient's Glasgow Coma Scale score also dropped from 15 to 13, indicating a slight decrease in neurological function.

Laboratory results showed an elevation in cardiac enzymes, with troponin I levels reaching 4 ng/mL (normal range 0-0.4 ng/mL), indicating ongoing myocardial damage. The patient's potassium level was also elevated at 5.7 mmol/L (normal range 3.5-5.1 mmol/L), which may have contributed to the irregular heart rhythm. Blood urea nitrogen and creatinine levels were also elevated, at 30 mg/dL (normal range 6-20 mg/dL) and 2.2 mg/dL (normal range 0.6-1.2 mg/dL) respectively, indicating worsening kidney function. This further complicated the patient's condition, as it could limit the types of medications that could be administered.

These findings necessitated a critical reevaluation of the patient's condition and a review of the management plan. The nurse immediately notified the healthcare team of the changes in the patient's status and prepared to implement more aggressive interventions, such as initiating a dopamine infusion to improve the patient's blood pressure and considering the use of an intra-aortic balloon pump to improve cardiac output. The nurse also initiated supplemental oxygen therapy to improve the patient's oxygen saturation levels. The patient's deteriorating condition required vigilant monitoring and swift action to prevent further complications.

Section 5

Change in Patient Status

Despite the aggressive interventions, the patient's condition continued to decline. The blood pressure remained low at 85/55 mmHg, and the pulse was still weak and irregular at 140 beats per minute, despite the dopamine infusion. Oxygen saturation improved slightly to 90% with the supplemental oxygen therapy but remained below the target of 94%. The patient's respiratory rate also remained elevated at 32 breaths per minute, with continued shallow respiration. The Glasgow Coma Scale score dropped further to 11, raising concerns about the patient's neurological state.

The patient's skin became cool and clammy, and the nurse noted a decrease in urine output to less than 30 mL per hour, indicating a decrease in renal perfusion. Additionally, the patient complained of worsening chest pain, rating it an 8 on a scale of 0 to 10. The patient also showed signs of increasing confusion and restlessness, which could be a symptom of decreased cerebral perfusion or hypoxia. These changes in the patient's status prompted the nurse to immediately notify the healthcare team and prepare to escalate care.