Pulmonic Stenosis - Nursing Case Study

Pathophysiology

• Primary mechanism: Pulmonic stenosis is characterized by a narrowing of the pulmonary valve in the heart. This results in an obstruction to blood flow from the right ventricle into the pulmonary artery, forcing the right ventricle to work harder to pump blood for oxygenation.

• Secondary mechanism: Over time, the increased workload causes hypertrophy (enlargement) of the right ventricle. This can lead to right-sided heart failure, as the ventricle struggles to maintain adequate blood flow.

• Key complication: Long-standing pulmonic stenosis may lead to arrhythmias as the electrical pathways in the thickened ventricle are disrupted. This can cause palpitations, lightheadedness, or even fainting.

Patient Profile

Demographics:

45-year-old male, construction worker

History:

• Diagnosed with mild Pulmonic Stenosis at the age of 30

• Currently on Furosemide and Beta-blockers

• No known allergies

Current Presentation:

• Chief complaint of increasing shortness of breath and fatigue

• Key symptoms include chest discomfort, fainting spells, and palpitations

• Vital signs: Blood Pressure: 130/85 mmHg, Pulse: 105 beats/min, Respiratory Rate: 22 breaths/min, Temperature: 98.6 F, Oxygen Saturation: 94% on room air.

Section 1

Change in Patient Status:

Over the next few days, the patient's condition began to deteriorate. He reported increased fatigue and his shortness of breath became more pronounced, even at rest. His oxygen saturation dropped to 89% on room air, and his respiratory rate increased to 28 breaths per minute. His pulse rate remained elevated at 115 beats per minute. The patient also began to experience edema in his ankles and lower legs, a common sign of right-sided heart failure. He also reported a decrease in urine output, which suggests that his kidneys may be affected by the reduced cardiac output.

New Diagnostic Results:

An Echocardiogram was performed and it demonstrated a significant increase in the thickness of the right ventricle, confirming the suspicion of right ventricular hypertrophy. The pulmonary valve appeared narrowed and the estimated pulmonary valve gradient was 60 mmHg, indicating severe pulmonic stenosis. In addition, an EKG showed occasional premature ventricular contractions (PVCs), which are often seen in patients with right ventricular hypertrophy and may be responsible for his palpitations. His B-type natriuretic peptide (BNP) level, a biomarker used to identify heart failure, was elevated at 900 pg/mL (normal range: <100 pg/mL). His renal function tests showed elevated creatinine and reduced glomerular filtration rate (GFR), indicating the onset of renal impairment likely secondary to the reduced cardiac output.

These findings suggest that the patient's pulmonic stenosis has progressed, leading to right ventricular hypertrophy and early signs of right-sided heart failure. The renal impairment also indicates that the heart failure may be affecting other organs. It is clear that the patient's condition is deteriorating and a more aggressive treatment approach may be needed.

Section 2

Response to Interventions:

Despite receiving diuretics and beta blockers to reduce the strain on his heart and decrease the edema, the patient's condition did not improve. His oxygen saturation dropped further to 85% on room air, prompting the need for supplemental oxygen. His respiratory rate remained elevated at 30 breaths per minute, and his pulse rate increased to 120 beats per minute, indicating persistent tachycardia. The edema in his lower legs worsened and he now started to complain of abdominal distension. His urine output continued to decrease, with less than 400 mL in 24 hours.

New Complications:

The patient's worsening condition and the increasing severity of his symptoms indicated the development of congestive heart failure. His abdominal distension, in combination with the increased edema, pointed towards the possibility of ascites, a condition in which fluid accumulates in the abdominal cavity, typically due to liver disease or heart failure. A diagnostic paracentesis was performed which confirmed the presence of ascites. In addition, his liver function tests were abnormal with elevated levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), suggesting that his liver was also being affected by the reduced cardiac output.

This case now illustrates the need for urgent intervention to manage the severe pulmonic stenosis, the heart failure, and the complications affecting the patient's kidneys and liver. A multidisciplinary approach involving cardiology, nephrology, and gastroenterology teams may be necessary for optimal management.

Section 3

Change in Patient Status:

Despite aggressive management, the patient's condition continued to deteriorate. His oxygen saturation levels remained low around 82% even with the supplemental oxygen. His pulse rate increased further to 135 beats per minute and his blood pressure dropped to 90/60 mmHg, indicating possible cardiogenic shock. He became increasingly lethargic and disoriented, suggesting that his brain was not receiving adequate oxygen supply.

New Complications:

A repeat abdominal ultrasound showed increased ascites, confirming that the diuretics were not effectively managing his fluid overload. His urine output further decreased to only 200 mL in 24 hours, suggesting worsening renal function. Lab results showed elevated blood urea nitrogen (BUN) and creatinine levels, confirming acute kidney injury. Moreover, liver function tests showed further elevations in ALT and AST levels, indicating worsening liver function. His prothrombin time (PT) and international normalized ratio (INR) were also elevated, suggesting a coagulation disorder likely due to liver dysfunction. These new complications indicate multi-organ failure secondary to the advanced heart failure, necessitating urgent reevaluation of the current management plan.

Section 4

Change in Patient Status:

Despite the medical team's efforts, the patient's condition worsened. His oxygen saturation levels dropped further to 79%, and his pulse rate escalated to 145 beats per minute. His blood pressure also fell to 85/55 mmHg, indicating a further decline into cardiogenic shock. His lethargy and disorientation intensified, suggesting continued inadequate oxygen supply to the brain.

New Complications:

Subsequent lab results showed a significant increase in the patient's blood urea nitrogen (BUN) and creatinine levels, indicating a further decline in renal function. His urine output decreased to a mere 150 mL over the next 24 hours. Moreover, his liver function tests showed a marked increase in ALT and AST levels, indicative of worsening liver dysfunction. His prothrombin time (PT) and international normalized ratio (INR) were also significantly elevated, suggesting a serious coagulation disorder secondary to the liver dysfunction. This patient is now showing signs of multi-organ failure, likely due to the severe heart failure. These developments demand immediate reevaluation and modification of the management plan.

These changes not only challenge the current management plan but also raises questions about other potential underlying issues that could be exacerbating the patient's condition. The team must now consider more aggressive interventions or potential surgical options to alleviate the heart's burden, manage fluid overload, and restore organ function.

Section 5

Change in Patient Status:

The patient's condition continued to deteriorate. His oxygen saturation levels plummeted to a critical 68%, and despite the administration of supplemental oxygen, there was no visible improvement. His pulse rate now fluctuated between 150 to 160 beats per minute. The blood pressure reading was alarmingly low at 75/45 mmHg, further indicating progression of cardiogenic shock. His state of consciousness significantly declined, and he became stuporous, indicating severe brain hypoxia.

New Complications:

The latest round of blood tests returned with alarming results. His BUN and creatinine levels had further increased, with values of 36 mg/dL and 3.6 mg/dL respectively, underscoring acute kidney injury. His decreased urine output of 100 mL over the past 24 hours corroborated this. Additionally, his liver function tests showed a further rise in ALT and AST levels, now reaching 250 U/L and 300 U/L respectively, indicating acute liver damage. His PT and INR values were also notably high at 18 seconds and 1.8 respectively, suggesting increased risk of bleeding. The patient was now in full-blown multi-organ failure, with renal and hepatic systems severely compromised. Immediate critical care interventions are necessary to prevent further deterioration and potential fatality.