Heart failure - Nursing Case Study

Pathophysiology

• Primary mechanism: Heart failure begins with a cardiac injury or stressor, such as high blood pressure or a heart attack, which damages heart muscle cells. This damage reduces the heart's pumping efficacy, leading to a compensatory response where the body tries to maintain cardiac output by enlarging the heart (cardiac remodeling), increasing heart rate, and retaining fluid.

• Secondary mechanism: Over time, these compensatory responses exacerbate heart failure. Enlargement of the heart and increased heart rate lead to further wear and tear on the heart muscle. Fluid retention increases the volume of blood the heart must pump, adding additional strain.

• Key complication: Chronic heart failure can lead to kidney damage. As cardiac output decreases, blood flow to the kidneys reduces, leading to fluid and sodium retention, and possibly renal failure. This exacerbates fluid overload, further straining the heart and perpetuating a vicious cycle.

Patient Profile

Demographics:

65-year-old male, retired construction worker

History:

• Key past medical history: Diagnosed with hypertension and type 2 diabetes

• Current medications: Metformin, Lisinopril, and Aspirin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Increasing shortness of breath and swelling in legs

• Key symptoms: Fatigue, rapid weight gain, persistent cough, decreased appetite

• Vital signs: Blood Pressure 150/95 mmHg, Pulse 110 bpm, Respiratory rate 24 breaths per minute, Oxygen Saturation 90% on room air, body mass index 30 kg/m2.

Section 1

New Diagnostic Results:

Upon admission, the patient was sent for an echocardiogram which revealed a decreased ejection fraction of 35%, indicative of a significant impairment in the heart's pumping ability. Additionally, laboratory results showed elevated B-type natriuretic peptide (BNP) levels at 900 pg/ml, which is consistent with heart failure. Furthermore, the patient had an elevated creatinine level of 1.8 mg/dL and a reduced estimated glomerular filtration rate (eGFR) of 45 ml/min/1.73 m2, suggesting the presence of moderate kidney dysfunction.

Change in Patient Status:

Over the next 24 hours, the patient's condition deteriorated. His shortness of breath became progressively worse, and he developed orthopnea, experiencing difficulty breathing while lying flat. His oxygen saturation dropped to 85% on room air, and his respiratory rate increased to 30 breaths per minute. His blood pressure also escalated to 160/100 mmHg, and his heart rate increased to 120 bpm. On physical examination, his jugular venous pressure was elevated and there was bilateral crepitation in the lungs, suggesting pulmonary congestion.

These new findings indicate that the patient's heart failure is worsening, potentially due to the additional stress on the kidneys. The clinical picture suggests a possible progression to acute decompensated heart failure, which requires immediate intervention to prevent further deterioration and organ damage. The elevated kidney function tests, worsening respiratory status, and signs of fluid overload all point towards this direction, necessitating an urgent re-evaluation of the patient's treatment plan.

Section 2

Response to Interventions:

In response to the patient's deteriorating condition, the medical team initiated intravenous administration of furosemide, an effective diuretic to reduce the fluid overload and alleviate the pulmonary congestion. A dose of 40 mg was given initially, and was followed up with 20 mg after six hours. Besides, the patient was also started on supplemental oxygen via nasal cannula at 2 liters per minute to improve his oxygen saturation, which subsequently increased to 92%.

However, despite these interventions, the patient's blood pressure remained high at 158/96 mmHg and his heart rate was still tachycardic at 112 bpm. Moreover, his respiratory rate remained elevated at 28 breaths per minute, indicating ongoing respiratory distress. These findings suggest that the initial interventions have not been fully effective in stabilizing the patient's condition. The healthcare team would need to reassess the patient's response to the ongoing treatment and consider other therapeutic options, such as the use of ACE inhibitors or beta-blockers, to control the patient's blood pressure and heart rate.

New Complications:

The next morning, the patient complained of increasing abdominal discomfort, and his abdomen appeared distended on physical examination. His urine output was also noted to have decreased to less than 30 mL/hour over the past 12 hours. A repeat lab test showed a further increase in his creatinine levels to 2.3 mg/dL, and his BNP levels remained elevated at 925 pg/ml. These clinical findings suggest a worsening of his renal function, likely due to the poor cardiac output and high systemic vascular resistance, further complicating the management of his heart failure. This new development calls for a careful reassessment of his fluid management strategy, including a possible adjustment in his diuretic therapy, to prevent further renal damage. Additionally, the patient might require a nephrology consult and possible renal replacement therapy if his renal function continues to decline.

Section 3

Change in patient status:

Over the next few hours, the patient's condition continued to deteriorate. He became increasingly dyspneic, even at rest, with a respiratory rate increasing to 36 breaths per minute and oxygen saturation dropping to 88% despite the supplemental oxygen therapy. The patient's blood pressure also spiked to 180/110 mmHg, and his heart rate remained tachycardic at 120 bpm. He also reported worsening abdominal discomfort along with nausea.

New diagnostic results:

An urgent echocardiogram was ordered which revealed an ejection fraction of 30%, confirming the diagnosis of heart failure with reduced ejection fraction (HFrEF). Furthermore, the repeat labs showed an alarming rise in creatinine levels to 3.0 mg/dL, indicating worsening renal function. The patient's BNP level had also escalated to 1100 pg/ml, reflecting the severity of his heart failure. Additionally, a chest X-ray was performed which indicated worsening pulmonary congestion. These findings indicate the patient's ongoing decompensation, necessitating immediate and aggressive interventions.

Section 4

Response to Interventions:

In response to the patient's deteriorating condition, the healthcare team decided to escalate his treatment plan. The patient was started on intravenous nitroglycerin to control his blood pressure and relieve his cardiac workload. His oxygen therapy was also increased to a non-rebreather mask, which improved his oxygen saturation to 92%. An IV loop diuretic was administered to reduce the fluid overload, while an ACE inhibitor was initiated to improve his heart function and renal perfusion.

However, the patient's response to these interventions was less than optimal. Although there was a slight improvement in his respiratory rate and oxygen saturation, his blood pressure remained high at 170/100 mmHg. His heart rate also continued to be elevated at 115 bpm, and his abdominal discomfort persisted. Moreover, alarmingly, the patient's urine output was minimal despite the diuretic therapy, suggesting a possible worsening of his renal function. This situation calls for a re-evaluation of the patient's management plan, possibly considering more potent antihypertensive agents or even renal replacement therapy.

Section 5

New diagnostic results:

Further diagnostic tests were performed to investigate the worsening renal function and persistent high blood pressure. A renal ultrasound showed increased echogenicity of the kidneys, indicating chronic kidney disease (CKD). Lab tests confirmed this with an elevated serum creatinine level of 3.0 mg/dL and a decreased estimated glomerular filtration rate (eGFR) of 35 mL/min/1.73 m2. The patient's serum potassium level was also elevated at 5.5 mEq/L, which could be contributing to his elevated heart rate.

In addition, an echocardiogram revealed that the patient's heart failure was more severe than initially thought. His ejection fraction was only 30%, indicating significant systolic dysfunction. The left ventricle also showed hypertrophy, which could explain his resistant high blood pressure. This new information necessitates a re-evaluation of the patient's treatment plan. It may require the addition of a beta-blocker to control his heart rate and blood pressure, and possibly the use of a potassium-wasting diuretic to correct his hyperkalemia. Also, the patient may require a referral to a nephrologist for management of his CKD.