heart failure - Nursing Case Study

Pathophysiology

• Primary mechanism: Reduced cardiac output due to weakened heart muscle. This is often caused by damage following a heart attack, or due to chronic conditions like hypertension or diabetes. The heart struggles to pump blood efficiently, leading to fluid build-up in lungs, liver, gut, and limbs.

• Secondary mechanism: Neurohormonal activation. As cardiac output declines, the body tries to compensate by activating the sympathetic nervous system and renin-angiotensin-aldosterone system (RAAS). This results in vasoconstriction, fluid retention, and further cardiac workload, worsening the heart failure.

• Key complication: Pulmonary edema. Due to the heart's reduced pumping ability, blood backs up into the veins that take blood through the lungs. As pressure in these blood vessels increases, fluid is pushed into the alveoli, causing shortness of breath.

Patient Profile

Demographics:

68-year-old male, retired construction worker.

History:

• Key past medical history: Diagnosed with hypertension and type 2 diabetes 10 years ago, previous myocardial infarction 5 years ago.

• Current medications: Metformin, Lisinopril, Aspirin, Atorvastatin.

• Allergies: Penicillin.

Current Presentation:

• Chief complaint: Increasing shortness of breath, especially during physical activities, and swelling in ankles and feet.

• Key symptoms: Fatigue, rapid or irregular heartbeat, persistent cough or wheezing with white or pink blood-tinged phlegm, decreased alertness or concentration.

• Vital signs: Blood pressure 140/90 mmHg, heart rate 100 bpm, respiratory rate 22 breaths per minute, SpO2 90% on room air, body mass index 28.

Section 1

Change in Patient Status:

Over the next 24 hours, the patient's condition continues to deteriorate. He becomes increasingly dyspneic, even at rest, and his SpO2 drops to 85% on room air. His heart rate rises to 110 bpm and his blood pressure increases to 150/95 mmHg. Auscultation of the lungs reveals crackles bilaterally, suggesting worsening pulmonary edema. The patient also reports increased fatigue and decreased urine output.

On physical examination, his jugular venous pressure is visibly elevated, indicating right heart failure. Pitting edema has extended from his ankles to his calves. Additionally, the patient has become less alert and is struggling to concentrate, suggesting possible cerebral hypoxia due to the reduced cardiac output. These clinical findings indicate the patient's heart failure is progressing to a more severe stage, requiring urgent intervention and possible escalation of care.

Section 2

New Diagnostic Results:

The attending physician orders a series of diagnostic tests including a complete blood count (CBC), basic metabolic panel (BMP), B-type natriuretic peptide (BNP), and an echocardiogram. Laboratory results reveal an elevated white blood cell count of 15,000/mm3, suggesting an ongoing infection. His BMP shows a decreased glomerular filtration rate (GFR) of 45 mL/min, indicating decreased renal function, likely due to decreased perfusion from the heart failure. His BNP levels are significantly elevated at 900 pg/mL, further confirming the diagnosis of heart failure.

The echocardiogram results show a decreased ejection fraction of 35%, indicating a reduced ability of the heart to pump blood effectively, and signs of enlargement and weakening of the right ventricle, consistent with right-sided heart failure. The echocardiogram also shows moderate regurgitation through the mitral valve, suggesting valve dysfunction as a possible contributing factor to the patient's worsening heart failure. These new results necessitate immediate medical management and further exploration of the cause of the patient's infection.

Section 3

Change in Patient Status:

Over the next few hours, the patient's condition deteriorates. His oxygen saturation levels drop to 88% on room air, and his respiratory rate increases to 24 breaths per minute. These changes suggest that the patient is developing hypoxemia, likely due to fluid accumulation in the lungs secondary to his heart failure. His blood pressure is also trending downwards, with current readings of 100/60 mmHg, a potential sign of decreasing cardiac output.

On physical examination, the patient appears increasingly dyspneic and reports increasing chest discomfort. Auscultation of his lungs reveals crackles in the lower lobes, indicating fluid accumulation. His lower extremities are markedly swollen, with pitting edema up to the knees, a sign of worsening right-sided heart failure. His urine output has also decreased to 20 mL/hour over the last 4 hours, further suggesting impaired renal perfusion. These changes in the patient's status necessitate immediate intervention to manage his worsening heart failure and potential sepsis from the ongoing infection.

Section 4

New Diagnostic Results:

Laboratory results return revealing the patient's B-type natriuretic peptide (BNP) level is elevated at 900 pg/mL, significantly above the normal range of less than 100 pg/mL, indicating severe heart failure. His Troponin I level is also above normal at 1.5 ng/mL, suggesting possible myocardial damage. The patient's blood cultures are positive for Staphylococcus aureus, confirming the presence of a systemic infection that could be exacerbating his heart failure.

Additionally, an EKG shows new-onset atrial fibrillation (AFib). This irregular and often rapid heart rate can lead to poor blood flow and further decrease cardiac output. A chest x-ray also reveals evidence of pulmonary edema, consistent with the patient's symptoms and physical examination findings. The combination of these results indicates that the patient's heart failure is worsening, and there is an urgent need to manage his cardiac function and infection simultaneously. These findings require a careful balance of fluid management to treat the patient's hypovolemia and avoid exacerbating his heart failure and pulmonary edema. The diagnostic results also suggest the need for anticoagulation to manage the patient's new-onset AFib and reduce the risk of stroke, but this decision will require careful consideration given the patient's already low blood pressure.

Section 5

Change in Patient Status:

Over the next few hours, the patient's condition continues to deteriorate. His heart rate increases to 130 beats per minute, and his blood pressure drops to 90/60 mmHg. His oxygen saturation falls to 88% on room air, and he is increasingly short of breath. On auscultation, his lung sounds reveal increased crackles bilaterally, indicative of worsening pulmonary edema. His level of consciousness also declines, and he becomes increasingly confused and disoriented, suggesting possible cerebral hypoperfusion due to the low cardiac output.

Additionally, his urine output has decreased to less than 30 mL per hour over the last 4 hours, suggesting possible renal hypoperfusion and acute kidney injury (AKI). This could be secondary to his heart failure exacerbation and/or sepsis. These changes in his status indicate that the patient's heart failure is worsening and now complicated by possible acute kidney injury and worsening systemic infection. The patient's new status necessitates urgent intervention to stabilize his hemodynamics, manage his fluid status, treat his infection, and minimize the risk of further organ damage.