heart disease - Nursing Case Study

Pathophysiology

• Primary mechanism: Atherosclerosis - This begins when the endothelium (innermost layer of arteries) gets damaged, enabling LDL cholesterol to infiltrate the artery wall and accumulate, forming plaques. Over time, these plaques harden and narrow the arteries, limiting oxygen-rich blood supply to the heart.

• Secondary mechanism: Inflammatory response - The body's immune response triggers inflammation around the plaque, making it unstable. If the plaque ruptures, it can form a clot that further blocks blood flow or breaks off and causes a blockage elsewhere, leading to a heart attack or stroke.

• Key complication: Ischemic heart disease - Chronic lack of oxygen due to reduced blood supply can lead to chest pain (angina), arrhythmias, or even heart failure, where the heart can't pump blood effectively. In acute cases, a sudden blockage can cause myocardial infarction (heart attack).

Patient Profile

Demographics:

62-year-old male, office worker

History:

• Key past medical history: Diagnosed with heart disease 5 years ago, hypertension, high cholesterol, sedentary lifestyle

• Current medications: Beta-blockers, statins, aspirin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Increasing episodes of chest pain, shortness of breath, fatigue

• Key symptoms: Intermittent chest pain worsening over the past month, shortness of breath especially on exertion, fatigue, occasional dizziness, unexplained weight gain, swelling in the ankles and feet

• Vital signs: Blood pressure 160/90 mmHg, pulse 95 bpm, respirations 20 per minute, oxygen saturation 92% on room air, temperature 98.6 degrees Fahrenheit

Section 1

New Diagnostic Results:

The patient's EKG shows ST-segment depression and T wave inversions, consistent with ischemia. His troponin levels came back elevated at 0.5 ng/mL, indicating possible myocardial injury. His lipid profile revealed LDL cholesterol of 160 mg/dL, HDL cholesterol of 35 mg/dL, total cholesterol of 240 mg/dL, and triglycerides of 200 mg/dL, all of which are higher than recommended levels. This lipid profile, along with his history of heart disease, hypertension, high cholesterol, and sedentary lifestyle, suggests a high risk of atherosclerosis progression and cardiovascular events.

An echocardiogram was performed, which showed left ventricular hypertrophy and decreased ejection fraction of 45%, suggestive of heart failure. The echocardiogram also confirmed the presence of moderate aortic stenosis. His B-type natriuretic peptide (BNP) was elevated at 600 pg/mL, which is consistent with heart failure.

These results indicate that the patient is experiencing a worsening of his heart disease, likely due to the progression of atherosclerosis and the development of heart failure. The elevated troponin level suggests a recent cardiac event, possibly a minor heart attack. These findings necessitate the reevaluation of his current treatment plan and the consideration of more aggressive interventions.

Section 2

Change in Patient Status:

The patient's condition started to deteriorate over the next 24 hours. He began experiencing increasing shortness of breath, even at rest, and reported chest discomfort and dizziness. His vital signs showed a blood pressure of 145/90 mmHg, pulse rate of 110 bpm, respiratory rate of 24 breaths/min, and an oxygen saturation of 88% on room air. His physical examination revealed jugular venous distension, bilateral rales in the lungs, and lower extremity edema, suggesting worsening heart failure and fluid overload.

Response to Interventions:

The medical team initiated intravenous diuretics to reduce the fluid overload and started him on supplemental oxygen to improve his oxygen saturation. Despite these interventions, the patient's dyspnea persisted and his oxygen saturation remained below 90%. The team also started him on a nitroglycerin drip to address his chest discomfort and control his blood pressure. His lipid-lowering medication was adjusted to target the elevated cholesterol levels and slow the progression of atherosclerosis. However, the persistent symptoms and unstable vital signs suggest that these interventions might not be sufficient and more aggressive measures may be needed.

Section 3

New Diagnostic Results:

On further diagnostic evaluation, the patient's laboratory data revealed a significant increase in his Brain Natriuretic Peptide (BNP) levels to 1250 pg/mL, indicating acute decompensated heart failure. His troponin levels also showed a slight rise, indicating some myocardial damage. An electrocardiogram (EKG) was performed, showing ST-segment depression in the inferior leads, suggesting ischemia. The echocardiogram revealed a reduced ejection fraction of 35%, indicating systolic dysfunction and confirming worsening heart failure.

Change in Patient Status:

Despite the ongoing interventions, the patient's condition further declined. He became increasingly tachypneic with a respiratory rate of 30 breaths/min, and his oxygen saturation dropped further to 84%. He also developed a new-onset irregular heart rate, suggestive of atrial fibrillation. His blood pressure increased to 155/95 mmHg, and he was still experiencing chest discomfort. The patient also reported increased fatigue and reduced urine output, suggesting possible renal impairment. These changes in the patient's status indicated the progression of his heart failure and the development of new complications, which required immediate attention and further escalation in his treatment plan.

Section 4

New Complications:

The patient's new onset of atrial fibrillation was a significant concern. This irregular heart rhythm could lead to blood pooling in the heart, increasing the risk of clot formation and subsequently, stroke. The patient's rising blood pressure was also a cause for concern, as it added additional strain on his already weakened heart. In addition, the patient's reduced urine output and mounting fatigue suggested the onset of cardiorenal syndrome, where the dysfunction of either the heart or kidneys can lead to failure of the other.

Response to Interventions:

The patient was immediately started on anticoagulation therapy to reduce the risk of stroke associated with atrial fibrillation. Cardiologists were consulted, who recommended the initiation of rate control therapy to help manage the patient's irregular heart rhythm. His hypertension was managed with titration of antihypertensive medications. For the suspected cardiorenal syndrome, a nephrologist was consulted. The patient was closely monitored for urine output, fluid balance and electrolytes. Despite these interventions, the patient's oxygen saturation remained low, and he was still experiencing chest discomfort. The medical team decided to escalate the care and transfer the patient to the intensive care unit (ICU) for more aggressive management. This decision was based on the increasing severity of his symptoms, the complexity of managing multiple organ dysfunction, and the need for closer monitoring.

Section 5

Change in Patient Status:

Over the next few hours in the ICU, the patient's condition continued to deteriorate. His urine output further decreased, indicating worsening kidney function. His blood pressure began to fluctuate, at times dangerously low and at other times alarmingly high. His oxygen saturation dropped to 88%, despite receiving supplemental oxygen. The patient complained of increasing chest discomfort and breathlessness, and his fatigue was notably worsening. Upon examination, his extremities were found to be cool and his pulse was irregular, indicating poor perfusion. He also had a new finding of bilateral crackles in the lower lobes of his lungs, suggestive of fluid overload or possible early congestive heart failure.

New Diagnostic Results:

Labs drawn showed elevated BUN and creatinine levels of 36 mg/dL and 2.8 mg/dL respectively, further indicating worsening renal function. His cardiac enzymes were also elevated with a troponin level of 0.8 ng/mL, suggesting ongoing heart muscle damage. The EKG showed persistent atrial fibrillation. A chest X-ray showed signs of fluid overload with vascular congestion and possible early signs of pulmonary edema. The team ordered an echocardiogram, which revealed decreased left ventricular ejection fraction of 30%, indicating significant heart failure. These findings, combined with the patient's clinical presentation, pointed towards the progression of cardiorenal syndrome and worsening heart failure.