CHF - Nursing Case Study

Pathophysiology

• Primary mechanism: CHF, or Congestive Heart Failure, is primarily caused by a weakening or stiffening of the heart muscles. This leads to a decrease in the heart's ability to pump blood efficiently, causing low cardiac output and an increase in blood pressure within the heart.

• Secondary mechanism: As a compensatory response to low cardiac output, the body releases hormones such as adrenaline, noradrenaline, and renin. These increase heart rate, blood vessel constriction, and fluid retention, exacerbating the heart's workload and further reducing its pumping efficiency.

• Key complication: Over time, the heart's inability to pump enough blood leads to fluid buildup in the lungs, liver, and other body tissues (edema), causing breathlessness, fatigue, and organ dysfunction – characteristic symptoms and complications of CHF.

Patient Profile

Demographics:

67-year-old male, retired truck driver

History:

• Key past medical history: Hypertension, Type 2 diabetes, previous myocardial infarction 5 years ago

• Current medications: Lisinopril, Metformin, Aspirin, Atorvastatin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Difficulty breathing, especially when lying flat and during physical activities

• Key symptoms: Persistent cough or wheezing with white or pink blood-tinged phlegm, increased need to urinate at night, rapid weight gain from fluid retention, swelling in ankles, legs and abdomen

• Vital signs: Blood pressure 145/90 mmHg, Heart rate 110 bpm, Respiratory rate 22 breaths per minute, Oxygen saturation 88% on room air, Body Mass Index 30.5 kg/m2

Section 1

New Diagnostic Results:

The patient's lab results indicated an elevated B-type natriuretic peptide (BNP) level of 850 pg/mL, which is indicative of heart failure. His chest x-ray demonstrated cardiomegaly and signs of pulmonary edema. Additionally, an echocardiogram was performed, showing an ejection fraction of 35%, further confirming the diagnosis of CHF. The patient's blood glucose was also elevated at 195 mg/dL and his HbA1c was 8.5%, indicating poor control of his diabetes.

Change in Patient Status:

Over the next day, the patient's condition began to worsen. His respiratory rate increased to 28 breaths per minute and his oxygen saturation dropped to 85% on room air. His blood pressure increased to 160/98 mmHg, and heart rate was now irregular at 120 bpm. He continued to complain of difficulty breathing and the swelling in his ankles and abdomen seemed more pronounced. The patient was also noted to be increasingly fatigued and was less responsive during interactions.

These new findings suggest that the patient's CHF is worsening, possibly due to poor control of his blood pressure and diabetes. The increased respiratory rate and decreased oxygen saturation could suggest that his pulmonary edema is worsening. This progression requires immediate medical intervention and adjustment of the patient's treatment plan.

Section 2

Response to Interventions:

The team immediately initiated oxygen therapy, increasing the patient's oxygen saturation to 92%. Despite this intervention, his respiratory rate remained high at 26 breaths per minute. The patient was started on intravenous Lasix to help reduce his fluid volume and alleviate some of the symptoms of his heart failure. A few hours post-initiation of Lasix, his urinary output increased to 600 mL over 2 hours, but unfortunately, his blood pressure remained elevated at 162/100 mmHg.

To manage his blood pressure and irregular heart rate, a beta-blocker was initiated. However, after the first dose, the patient's heart rate decreased to 50 bpm and his blood pressure decreased to 100/60 mmHg. He reported feeling dizzy when trying to stand up. This situation raised concerns about the patient's sensitivity to the beta-blocker and the need for careful monitoring and possible dose adjustment. Meanwhile, his blood glucose levels remained high, and insulin management was initiated to achieve better glycemic control.

These responses to interventions indicate that while some progress is being made in managing the patient's CHF, the patient's condition remains unstable. His sensitivity to the beta-blocker and uncontrolled diabetes present additional challenges in managing his condition effectively. This situation requires ongoing clinical reasoning and potential modification of the treatment plan based on the patient's responses.

Section 3

New Diagnostic Results:

Early the following morning, the patient's lab results were returned. The patient's brain natriuretic peptide (BNP) levels were elevated at 900 pg/mL, indicating worsening heart failure. Additionally, his hemoglobin A1C was at 8.5%, reflecting poor glycemic control over the past few months. His renal function had also declined, with a serum creatinine of 2.3 mg/dL and a glomerular filtration rate (GFR) of 40 mL/min/1.73m².

His electrolytes were also imbalanced with a noted hypokalemia at 3.2 mmol/L, likely a result of the Lasix administration. This could potentially exacerbate his irregular heart rhythm. His liver function tests also came back slightly elevated, with his alanine aminotransferase (ALT) at 70 U/L and his aspartate aminotransferase (AST) at 80 U/L, indicating possible liver damage or stress.

These new diagnostic results provide additional challenges in managing the patient's condition. The renal impairment could potentially limit the use of certain heart failure medications and the hypokalemia could worsen his cardiac condition. Furthermore, the high BNP value confirms the worsening of his heart failure and the need for close monitoring and potential medication adjustments. The elevated liver enzymes and poor glycemic control also complicate the patient's management, requiring a careful balance of medications to avoid further organ damage. These results require careful interpretation and clinical reasoning to adjust the patient's treatment plan accordingly.

Section 4

Later that afternoon, the patient's condition started to deteriorate. He complained of increased shortness of breath and the nurses noted a decrease in his urine output. On assessment, he was found to be increasingly tachypneic with a respiratory rate of 28 breaths per minute, and his oxygen saturation had dropped to 88% on room air. His blood pressure was also elevated at 160/90 mmHg. On auscultation, there were crackles heard in the lower lung fields bilaterally, indicating fluid retention in the lungs, a sign of worsening CHF. His peripheral edema had also worsened, and his weight had increased by 2kg in the last 24 hours.

An urgent repeat BNP was sent, which came back at 1200 pg/mL, further confirming the worsening of his heart failure. The nursing team promptly initiated oxygen therapy, and his saturation improved to 94%. The healthcare provider was notified and ordered an increase in his Lasix to help manage his fluid retention. However, the provider also expressed concern about the potential impact on his renal function and potassium levels, given his already compromised renal function and hypokalemia. He ordered a repeat renal function test and serum potassium to be done first thing in the morning. The patient's deteriorating condition calls for a careful and precise balance in his treatment plan, taking into account his renal function, potassium level, and the worsening CHF.

Section 5

Overnight, the patient's condition remained unstable. He had periods of restlessness and was frequently roused due to his persistent shortness of breath. He was given 2mg of morphine for comfort and to help ease his respiratory distress. The morning nurse found him to be increasingly lethargic, with a Glasgow Coma Scale of 13/15. His oxygen saturation was 92% on 3L of oxygen via nasal cannula. His blood pressure remained elevated at 158/92 mmHg, and his pulse was irregular at a rate of 102 beats per minute. His respiratory rate remained high at 26 breaths per minute, and his temperature was 37.6°C. The nurse was particularly concerned about his diminished urine output overnight, which was just 200mL.

The lab results came back with a serum potassium of 2.8 mEq/L, indicating further worsening of his hypokalemia. His renal function had also deteriorated with a creatinine of 2.5 mg/dL and a GFR of 30 mL/min/1.73m^2, signifying a decline in his renal function. The healthcare provider was immediately informed of the patient's status and the lab results. These findings highlight the complex balancing act in managing this patient's condition, demonstrating the intricate interplay between the heart, kidneys, and electrolyte balance. The healthcare provider ordered an ECG to rule out arrhythmia due to hypokalemia, and a potassium supplement was prescribed. A renal ultrasound was also ordered to further investigate the cause of his worsening renal function. The nursing team continued to monitor his vital signs, fluid balance, and cardiac status closely, prepared to initiate further interventions as needed.