CHF - Nursing Case Study

Pathophysiology

• Primary mechanism: CHF, or congestive heart failure, primarily occurs due to the inability of the heart to pump sufficient blood to meet the body's needs. This can be due to weakened heart muscles (systolic dysfunction) or stiff heart muscles that can't fill properly (diastolic dysfunction).

• Secondary mechanism: Over time, the heart tries to compensate by enlarging (cardiac remodeling), increasing muscle mass (hypertrophy), and pumping faster (tachycardia). However, these compensatory mechanisms further weaken the heart and increase the risk of arrhythmias, leading to a vicious cycle of worsening heart failure.

• Key complication: Fluid overload is a common complication in CHF. As the heart's effectiveness decreases, blood backs up in the veins, causing fluid to accumulate in the tissues (edema), lungs (pulmonary congestion), and other organs, leading to additional symptoms and complications.

Patient Profile

Demographics:

72-year-old male, retired construction worker

History:

• Key past medical history: Hypertension, Type 2 Diabetes, Mild Congestive Heart Failure diagnosed 5 years ago

• Current medications: Amlodipine, Metformin, Carvedilol, Furosemide

• Allergies: Penicillin, Ibuprofen

Current Presentation:

• Chief complaint: Increased shortness of breath, fatigue, and swelling in the legs

• Key symptoms: Dyspnea on exertion, paroxysmal nocturnal dyspnea, orthopnea, bilateral ankle edema, fatigue, reduced exercise tolerance, persistent cough with frothy sputum

• Vital signs: Blood pressure 140/90 mmHg, pulse 96 bpm, respiratory rate 22 breaths/min, oxygen saturation 90% on room air, temperature 98.6 F.

Section 1

New Diagnostic Results:

The patient's lab results have returned with some concerning findings. His B-type Natriuretic Peptide (BNP) level is elevated at 890 pg/mL, indicating worsening heart failure. His chest X-ray shows cardiomegaly and pulmonary congestion, which aligns with his symptoms of dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. His electrocardiogram (ECG) shows atrial fibrillation (AFib), a common arrhythmia in patients with CHF that can further compromise cardiac output. This new finding requires careful assessment of his anticoagulation status given his increased risk of thromboembolism due to AFib. The patient's blood glucose level is also elevated at 180 mg/dL, possibly due to the stress of his worsening heart condition or poor control of his diabetes.

Change in Patient Status:

Over the next few hours, the patient's condition seems to deteriorate. His dyspnea worsens, and he is now having difficulty speaking in full sentences. His oxygen saturation drops to 86% on room air, and he appears more fatigued. His respiratory rate is now 28 breaths/min, pulse has increased to 110 bpm, and his blood pressure is 150/95 mmHg. The patient's ankles are significantly more swollen than before, and he complains of increased discomfort. He also reports feeling "fluttering" in his chest, likely associated with his new onset AFib. These changes suggest that his CHF is worsening, and immediate intervention is needed to prevent further decompensation.

Section 2

New Complications:

The nurse returns to reassess the patient and finds him to be increasingly restless and anxious, reporting a sense of impending doom. His dyspnea has worsened even further, with a respiratory rate now 35 breaths/min, and he is using accessory muscles to breathe. His oxygen saturation has dropped further to 80% on room air. Auscultation of his lungs reveals bilateral crackles extending up to the mid-thoracic level, suggesting fluid overload and possible acute pulmonary edema, a severe complication of CHF. His heart rate has increased to 120 bpm and blood pressure has risen to 160/100 mmHg.

The patient's urine output has also decreased significantly over the past few hours, with only 200 mL recorded, suggesting worsening renal perfusion due to decreased cardiac output. His blood glucose level has also risen to 220 mg/dL, indicating the need for tighter glycemic control. Furthermore, the patient is now complaining of a sudden onset, severe headache. His Glasgow Coma Scale (GCS) score is 14/15, down from 15/15 earlier, signifying a possible change in his neurological status. These new complications indicate a critical deterioration in the patient's condition, requiring immediate medical intervention and careful nursing management.

Section 3

New Diagnostic Results:

The nurse quickly orders a chest x-ray, which shows bilateral pulmonary infiltrates, consistent with the suspicion of acute pulmonary edema. The lab results reveal a B-type natriuretic peptide (BNP) level of 900 pg/mL, significantly elevated from his baseline, confirming the worsening of his CHF. His arterial blood gas (ABG) results show a pH of 7.30, partial pressure of carbon dioxide (PaCO2) of 55 mmHg, and a partial pressure of oxygen (PaO2) of 60 mmHg, indicating acute respiratory acidosis and hypoxemia.

The results of the renal function tests show increased creatinine (2.5 mg/dL) and blood urea nitrogen (BUN) levels (40 mg/dL), reflecting decreased renal perfusion. His hemoglobin A1C is 8.5%, indicating poor glycemic control over the past three months. Notably, his troponin levels have also risen to 0.5 ng/mL, which could suggest myocardial injury. The nurse realizes that these diagnostic results indicate a need for prompt medical intervention and a change in the patient's management plan.

Section 4

Change in Patient Status:

Over the next few hours, the patient's condition continues to deteriorate. He becomes increasingly short of breath even at rest, and his respiratory rate escalates to 28 breaths per minute. On auscultation, crackles are heard bilaterally in the lower lobes, and wheezing is noted on expiration. His oxygen saturation drops to 88% on room air, and he is put on 4 liters of oxygen via nasal cannula, which marginally improves his oxygen saturation to 92%.

His blood pressure has risen to 160/90 mmHg, and his heart rate is irregular at 110 beats per minute. His urine output has declined to less than 30 mL/hour over the past three hours, suggesting worsening renal function. On examination, his lower extremities are notably edematous, and jugular venous distension is observed. The nurse also notes that the patient appears anxious and reports feeling "a sense of impending doom." The nurse quickly informs the healthcare provider of the patient's deteriorating condition, indicating the need for urgent medical management to prevent further complications.

Section 5

New Diagnostic Results:

The healthcare provider promptly orders a set of labs, including a complete blood count (CBC), basic metabolic panel (BMP), and brain natriuretic peptide (BNP). The results reveal a slight elevation in the white blood cell count (12,000 cells/mcL), suggesting a possible infection. The BMP shows a rise in blood urea nitrogen (BUN) to 28 mg/dL and creatinine to 1.8 mg/dL, indicating a decline in renal function. The BNP, which is a marker for heart failure, is markedly elevated at 900 pg/mL, confirming the exacerbation of congestive heart failure. An electrocardiogram (EKG) is also performed, which reveals atrial fibrillation (AFib) - a possible cause for the irregular heartbeat.

The healthcare provider also orders a chest X-ray, which shows increased vascular markings and fluid in the lower lung fields, consistent with pulmonary edema. A bedside echocardiogram reveals a reduced ejection fraction of 35%, further validating the diagnosis of decompensated heart failure. The patient's worsening condition, combined with the diagnostic results, calls for immediate intervention to manage the heart failure and address the potential infection and declining renal function. The nurse anticipates the need for medications to control the heart rate, diuretics to manage fluid overload, and potential antibiotics to treat the suspected infection. The nurse also expects the healthcare provider to order continuous cardiac monitoring to track the patient's heart rhythm and rate.