heart failure - Nursing Case Study

Pathophysiology

• Primary mechanism: Reduced cardiac output - Heart failure begins when the heart can't pump sufficient blood to meet the body's needs, often due to weakened or stiff heart muscles. This results in reduced ejection fraction, leading to symptoms like fatigue and shortness of breath.

• Secondary mechanism: Neurohormonal activation - In response to reduced cardiac output, the body increases production of hormones like adrenaline and aldosterone. This causes fluid retention, increased heart rate and blood vessel constriction, worsening the heart's workload.

• Key complication: Fluid overload - The body's response to heart failure can lead to fluid buildup, or edema. This excess fluid often accumulates in the lungs (pulmonary edema), causing breathlessness, or in the legs and abdomen, causing swelling and discomfort.

Patient Profile

Demographics:

67-year-old male, retired construction worker

History:

• Key past medical history: Hypertension, Type 2 Diabetes Mellitus, previous myocardial infarction

• Current medications: Metformin, Lisinopril, Aspirin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Shortness of breath, fatigue after minor physical activity

• Key symptoms: Persistent cough or wheezing, swelling in feet, ankles, stomach and noticeable weight gain due to fluid retention, decreased alertness or concentration

• Vital signs: Blood pressure 160/90 mmHg, pulse 105 bpm, respiratory rate 26 breaths per minute, oxygen saturation 88% on room air, body mass index 30.5 kg/m2

Section 1

Change in Patient Status:

Over the course of the day, the patient's shortness of breath has worsened. He's now dyspneic at rest and his oxygen saturation has dropped to 85% despite receiving supplemental oxygen at 2L via nasal cannula. He also reports increasing abdominal discomfort and his legs appear more swollen than before. On auscultation, rales are heard in the lower lobes of both lungs, and his heart sounds reveal a gallop rhythm. His blood pressure has risen to 170/95 mmHg and pulse is now 118 bpm.

New Diagnostic Results:

Given the worsening of his symptoms, a decision is made to conduct further investigations. A chest X-ray reveals evidence of pulmonary edema, with an enlarged cardiac silhouette suggestive of cardiomegaly. His blood tests show a B-type Natriuretic Peptide (BNP) of 900 pg/ml, elevated from a baseline of 100 pg/ml, indicating worsening heart failure. His serum creatinine has also risen from 1.2 mg/dl to 1.8 mg/dl, suggesting possible kidney injury due to reduced perfusion. His Hemoglobin A1c is found to be 8.5%, indicating poorly controlled diabetes.

These findings suggest a worsening of the patient's heart failure, likely due to a combination of factors including uncontrolled hypertension, poorly managed diabetes, and possible non-compliance with medication. The challenge now is to stabilize the patient, optimize his fluid status, and address the underlying factors contributing to his decompensation.

Section 2

Response to Interventions:

Given the severity of the patient's condition, the medical team decides to increase the supplemental oxygen to 4L via nasal cannula to improve his oxygen saturation. However, despite this intervention, his oxygen saturation only increases to 88%. The patient is then started on a noninvasive positive pressure ventilation (NIPPV) to help improve his oxygenation and alleviate his dyspnea. After an hour on NIPPV, his oxygen saturation improves to 92%.

To address the patient's fluid overload and alleviate the symptoms of pulmonary edema, a loop diuretic, furosemide, is administered intravenously. The patient's urinary output is monitored closely, and within the next few hours, there's an increase in urine output. However, his blood pressure reduces to 150/85 mmHg, and he still reports feeling breathless.

The elevation in his blood pressure and heart rate, along with the presence of a gallop rhythm, suggest that the patient's heart is working harder to pump blood. An angiotensin-converting enzyme (ACE) inhibitor is started to reduce the workload on the heart and lower his blood pressure. However, the patient's BNP remains elevated at 850 pg/ml, indicating that his heart failure is yet to be adequately controlled.

This phase of the patient's treatment highlights the complexity of managing heart failure, particularly when it's complicated by other comorbidities. It also emphasizes the need for close monitoring and adaptation of treatment strategies in response to the patient's changing condition.

Section 3

On the third day of the patient's hospitalization, there is an abrupt change in his status. He reports a sudden onset of severe chest pain, radiating to the left arm. He appears visibly distressed, diaphoretic and his skin is pale. His blood pressure drops to 110/70 mmHg, and his heart rate increases to 120 bpm, further compounding the concern. The EKG shows new ST-segment elevations in the anterior leads, indicating an acute myocardial infarction (AMI).

The medical team reacts promptly, administering nitroglycerin for the chest pain and aspirin to limit the size of the infarction. He is also started on a heparin drip as part of the acute coronary syndrome management protocol. A stat troponin level is drawn, which comes back significantly elevated at 4.3 ng/ml, confirming the AMI diagnosis. The cardiology team is consulted, and the patient is quickly transferred to the catheterization lab for an emergent percutaneous coronary intervention (PCI).

This sudden turn of events underscores the vulnerability of patients with heart failure, who are at a higher risk of developing coronary artery disease and subsequent myocardial infarction. The development of AMI in this patient not only complicates his heart failure management but also necessitates a shift in the treatment strategy towards stabilizing the acute event. The situation demands intense clinical reasoning to prioritize interventions that address both the acute infarction and ongoing heart failure.

Section 4

During the PCI, it is observed that there is a 90% occlusion in the left anterior descending (LAD) artery. A drug-eluting stent is successfully placed, restoring blood flow to the affected myocardium. After the procedure, the patient is transferred to the coronary care unit (CCU) for close monitoring. His vital signs stabilize initially; however, on the fourth day post-PCI, the patient complains of increasing shortness of breath. On examination, crackles are heard bilaterally in the lower lung fields, and his oxygen saturation drops to 88% on room air.

Following these findings, a chest X-ray is ordered which shows bilateral infiltrates, suggestive of pulmonary edema. Blood gas analysis reveals a PaO2 of 60 mmHg and a PaCO2 of 32 mmHg, indicating hypoxemia and respiratory alkalosis, common in acute heart failure exacerbation. Additionally, B-type Natriuretic Peptide (BNP) levels are elevated at 1100 pg/ml, further corroborating the suspicion of acute heart failure.

This new development presents a complex clinical scenario. The patient’s recent AMI and PCI have likely exacerbated his pre-existing heart failure, leading to acute decompensation and pulmonary edema. The challenge now lies in managing the acute heart failure while ensuring the stability of his post-PCI condition. The team must weigh the risks and benefits of aggressive diuretic therapy, which could potentially compromise renal function, versus the need to rapidly relieve symptoms and improve oxygenation.

Section 5

The patient's condition continues to deteriorate over the next 24 hours, with an increase in dyspnea and worsening oxygen saturation, dropping to 84% on room air. His vital signs show a blood pressure of 96/60 mmHg, heart rate of 110 beats per minute, respiratory rate of 26 breaths per minute, and a temperature of 98.6°F. On cardiovascular examination, there is a new S3 gallop, and jugular venous distention is noted. His lower extremities show 2+ pitting edema bilaterally, which was not present prior to the PCI.

To gain further insight into the patient's deteriorating condition, a comprehensive set of labs are ordered. His serum creatinine level has increased from 1.2 mg/dl to 2.0 mg/dl over the past 24 hours, suggesting worsening renal function. Cardiac biomarkers, including troponin I, are also elevated at 0.5 ng/ml, which may suggest ongoing myocardial injury or stress. The ECG shows signs of a new left bundle branch block, which was not present in the previous ECG. This new development can impair cardiac output and lead to further decompensation of heart failure, adding another layer of complexity to the clinical picture. The team must now consider the implications of these new findings and devise a plan that addresses both the patient's acute heart failure and the new cardiac and renal complications.