Congestive Cardiac Failure - Nursing Case Study

Pathophysiology

• Primary mechanism: Impaired cardiac contractility reduces the heart's ability to pump blood effectively, leading to decreased cardiac output and subsequent tissue hypoperfusion. This triggers compensatory mechanisms like increased heart rate and ventricular dilation, which can further stress the heart muscle.

• Secondary mechanism: Fluid retention occurs due to activation of the renin-angiotensin-aldosterone system (RAAS), leading to increased blood volume and venous return. This exacerbates the workload on an already weakened heart, contributing to congestion in the pulmonary and systemic circulation.

• Key complication: Pulmonary congestion arises from fluid back-up in the lungs, resulting in symptoms such as dyspnea and orthopnea, making effective management crucial to prevent respiratory distress and maintain oxygenation.

Patient Profile

Demographics:

65-year-old female, retired school teacher

History:

• Key past medical history: Hypertension, Type 2 Diabetes Mellitus, Hyperlipidemia

• Current medications: Lisinopril, Metformin, Atorvastatin, Furosemide

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Increasing shortness of breath

• Key symptoms: Fatigue, orthopnea, paroxysmal nocturnal dyspnea, swelling in legs

• Vital signs: Blood pressure 145/90 mmHg, heart rate 105 bpm, respiratory rate 24 breaths/min, temperature 37.2°C, oxygen saturation 88% on room air

Section 1

As the healthcare team conducted an initial assessment, they noted several important findings that indicated worsening congestive cardiac failure. The patient presented with an increased respiratory rate of 28 breaths per minute, and her oxygen saturation had decreased further to 85% despite being placed on supplemental oxygen at 2 liters via nasal cannula. Auscultation of the lungs revealed bilateral coarse crackles, particularly in the lower lobes, suggesting significant pulmonary congestion. Peripheral edema had also worsened, with pitting edema now extending up to the knees.

Laboratory tests revealed elevated B-type natriuretic peptide (BNP) levels at 1,200 pg/mL, indicating significant cardiac stress and volume overload. Serum electrolytes showed hyponatremia with a sodium level of 130 mmol/L, likely a result of dilutional effects from fluid retention and ongoing diuretic therapy. The patient's renal function was also compromised, with a serum creatinine of 1.8 mg/dL, highlighting the impact of both heart failure and diuretic use on renal perfusion. This data suggested a critical need to optimize fluid balance and relieve cardiac workload while closely monitoring renal function.

These findings prompted the healthcare team to consider adjusting her treatment plan, potentially increasing the dose of diuretics and initiating a low-dose beta-blocker to manage heart rate and improve cardiac efficiency. The team also discussed the importance of dietary sodium restriction and fluid management with the patient to help manage her symptoms. This comprehensive approach aimed to stabilize her condition, prevent further complications, and improve her quality of life, all while ensuring close monitoring of her renal function and electrolyte balance.

Section 2

Two days after the adjustments in the treatment plan, the healthcare team conducted a follow-up assessment to evaluate the patient's response to the interventions. Initially, there seemed to be a slight improvement in respiratory status; her respiratory rate had decreased to 24 breaths per minute, and her oxygen saturation modestly improved to 88% on 2 liters of supplemental oxygen. However, the patient still complained of significant shortness of breath, particularly during minimal exertion, such as attempting to walk to the bathroom. Lung auscultation continued to reveal coarse crackles, indicating persistent pulmonary congestion.

The team noted a concerning rise in the patient's heart rate to 110 beats per minute, alongside an irregular rhythm detected during auscultation, suggestive of the development of atrial fibrillation. This new arrhythmia could exacerbate her heart failure by reducing cardiac output and increasing cardiac workload. To confirm this, an electrocardiogram (ECG) was ordered, which indeed confirmed the presence of atrial fibrillation. This change in cardiac rhythm posed a new challenge, as it could further reduce her cardiac efficiency and potentially lead to thromboembolic complications.

Laboratory results showed a continued trend of hyponatremia, with sodium levels now at 128 mmol/L, and a slight worsening of renal function, with serum creatinine increasing to 2.0 mg/dL. These findings highlighted the delicate balance required in managing fluid status and diuretic therapy. The healthcare team deliberated on adjusting her medication regimen to address the atrial fibrillation, considering options such as anticoagulation to reduce the risk of stroke and the introduction of rate-controlling medications like digoxin or a higher dose of beta-blockers, though these would need to be carefully balanced with her renal status and electrolyte disturbances. The patient and her family were informed about the new developments, emphasizing the importance of closely monitoring her symptoms and maintaining rigorous follow-up appointments to manage these complexities effectively.

Section 3

Despite the recent changes in the treatment plan, the patient's condition continued to evolve, presenting new challenges for the healthcare team. During a subsequent assessment, the patient's respiratory rate increased again to 28 breaths per minute, and her oxygen saturation dropped to 85% on 2 liters of supplemental oxygen, indicating a worsening of her pulmonary congestion. Her heart rate remained elevated at 115 beats per minute with persistent irregularity, confirming ongoing atrial fibrillation. This increased cardiac workload was concerning, especially given the patient's fragile state. The team also noted a mild increase in her blood pressure, now reading 150/95 mmHg, which could further strain her compromised cardiovascular system.

Further laboratory tests revealed a persistent decline in renal function, with serum creatinine rising to 2.3 mg/dL and blood urea nitrogen (BUN) increasing to 48 mg/dL. These results suggested that the kidneys were struggling, likely due to the combination of decreased cardiac output and the effects of diuretic therapy. Additionally, her sodium levels slightly improved, now at 130 mmol/L, but remained below the normal range, indicating ongoing challenges in managing her fluid and electrolyte balance. The healthcare team was faced with the critical task of optimizing her heart failure management while mitigating the risk of further renal impairment.

In response to these developments, the team decided to initiate anticoagulation therapy with low-dose rivaroxaban to reduce the risk of stroke associated with atrial fibrillation. They also opted to adjust her diuretic regimen, transitioning to a lower dose of loop diuretics and introducing an angiotensin receptor-neprilysin inhibitor (ARNI) to improve her cardiac output and renal perfusion. The patient was closely monitored for any signs of bleeding or further electrolyte disturbances. The healthcare team emphasized the importance of adherence to the new medication regimen and scheduled a follow-up visit in 48 hours to reassess her clinical status and adjust the treatment plan as necessary.

Section 4

During the follow-up visit 48 hours later, the healthcare team conducted a thorough assessment to evaluate the patient's response to the recent interventions. Encouragingly, her respiratory rate had decreased to 22 breaths per minute, and her oxygen saturation had improved to 90% on 2 liters of supplemental oxygen, suggesting some alleviation of pulmonary congestion. The heart rate remained elevated at 110 beats per minute, but with a more regular rhythm, indicating a partial improvement in her atrial fibrillation management. However, her blood pressure remained elevated at 148/92 mmHg, which continued to pose a risk for her cardiovascular health.

Laboratory tests showed a slight improvement in renal function, with serum creatinine decreased to 2.1 mg/dL and BUN reduced to 44 mg/dL. These changes suggested that the modifications to her diuretic regimen and the introduction of the ARNI were beginning to have a positive effect on her renal perfusion and overall fluid balance. Sodium levels remained stable at 131 mmol/L, indicating that the team was successfully managing her electrolyte balance thus far. However, there was a new concern: her hemoglobin levels had dropped to 10.5 g/dL from 11.8 g/dL, raising the possibility of bleeding as a complication of anticoagulation therapy.

Clinically, the patient reported feeling slightly more energetic and less short of breath, though she still experienced occasional dizziness and fatigue. The healthcare team recognized the need to closely monitor her hemoglobin levels and any potential signs of bleeding, while also continuing to optimize her heart failure management. They scheduled another follow-up visit in 72 hours to reassess her clinical status, with a particular focus on her hematologic profile and overall stability. The team remained vigilant, ready to make further adjustments to her treatment plan to prevent any new complications and to support her ongoing recovery.

Section 5

During the next follow-up visit, the healthcare team conducted a comprehensive assessment to evaluate the patient's current status and response to ongoing treatment. Upon examination, the patient's vital signs indicated a mixed response to the interventions. Her respiratory rate had stabilized further at 20 breaths per minute, and her oxygen saturation had improved slightly to 92% on 2 liters of supplemental oxygen, demonstrating continued progress in resolving pulmonary congestion. However, her heart rate remained elevated at 108 beats per minute, and while she was in sinus rhythm, there was a concern about persistent tachycardia. Blood pressure was measured at 150/94 mmHg, indicating a need for further optimization of her antihypertensive regimen.

Laboratory tests revealed new diagnostic results that warranted attention. Her hemoglobin had dropped further to 9.8 g/dL, increasing the suspicion of occult bleeding, potentially linked to her anticoagulation therapy. The team decided to perform a fecal occult blood test, which returned positive, confirming gastrointestinal bleeding as a likely cause of her anemia. This necessitated immediate adjustments to her anticoagulant dosing to balance the risk of thromboembolism with the need to manage her bleeding risk effectively. Additionally, her renal function showed continued improvement, with serum creatinine at 1.9 mg/dL and BUN at 40 mg/dL, suggesting that her fluid and electrolyte management was being effectively handled.

The patient reported feeling more fatigued and had noticed dark, tarry stools, which supported the clinical findings of gastrointestinal bleeding. The team promptly initiated a gastroenterology consult to evaluate the source of bleeding and planned for an upper endoscopy to identify and potentially treat the bleeding site. Meanwhile, they reduced the dose of her anticoagulant and initiated iron supplementation to address her anemia. These steps were crucial in stabilizing her hematologic status while maintaining her overall cardiovascular management. The team remained vigilant, understanding that her complex condition required careful and continuous monitoring to avoid further complications and to guide her toward a stable recovery.