Truncus Arteriosus - Nursing Case Study

Pathophysiology

• Primary mechanism: Truncus arteriosus is a congenital heart defect where a single large blood vessel, instead of separate aorta and pulmonary arteries, emerges from the heart. This single vessel supplies both oxygenated and deoxygenated blood to the body and lungs, causing mixing of oxygen-rich and oxygen-poor blood.

• Secondary mechanism: A ventricular septal defect is usually present, allowing more blood to mix. This results in an excessive volume of blood being sent to the lungs, leading to pulmonary hypertension.

• Key complication: The heart works harder to pump blood, resulting in heart failure. The increased blood flow to the lungs also leads to their damage over time. These complications can result in poor growth, respiratory infections, and decreased exercise tolerance.

Patient Profile

Demographics:

2-year-old male, not applicable for occupation

History:

• Born with Truncus Arteriosus, underwent a successful surgical repair at 2 months old

• Currently on Furosemide and Captopril

• No known drug allergies

Current Presentation:

• Chief complaint: Persistent cough and difficulty in feeding

• Key symptoms: Wheezing, rapid breathing, fatigue, and poor weight gain

• Vital signs: Heart rate - 160 bpm, Respiratory rate - 55 breaths per minute, Blood Pressure - 90/50 mmHg, Temperature - 98.6°F, Oxygen Saturation - 88% on room air.

Section 1

Change in Patient Status:

Over the next 24 hours, the patient's condition deteriorates. His heart rate increases to 180 bpm, respiratory rate to 65 breaths per minute, and his oxygen saturation drops to 82% on room air. He also becomes increasingly lethargic and shows signs of significant distress during feeds. His cough becomes more frequent and is accompanied by increased wheezing.

The nurse notices a new, harsh, holosystolic murmur on auscultation of the chest, suggestive of worsening ventricular septal defect and increased pulmonary blood flow. The patient also develops edema in his lower extremities, indicative of worsening heart failure. These findings suggest the possibility of a complication related to his underlying condition, such as stenosis or regurgitation at the site of his previous surgical repair, or progression of his pulmonary hypertension.

This situation requires immediate medical evaluation and intervention. The nurse should prioritize communication with the healthcare team about the patient's change in status, and prepare for potential diagnostic procedures or therapeutic interventions such as diuretic therapy increase or introduction of new heart failure medications. This case highlights the importance of ongoing assessment and prompt recognition of clinical deterioration in patients with complex congenital heart disease.

Section 2

Change in Patient Status:

As the nurse continues to monitor the patient over the next few hours, he remains tachycardic with a heart rate fluctuating between 170-190 bpm. His respiratory rate continues to be elevated at 70 breaths per minute, and his oxygen saturation levels remain low, hovering around 80% on room air. In addition, the patient's level of consciousness decreases, and he becomes increasingly unresponsive, only responding to painful stimuli. His skin appears dusky and mottled, and his extremity edema worsens. His cough remains persistent with increased wheezing and the nurse also notes new onset of grunting and use of accessory muscles.

New Diagnostic Results:

The healthcare team orders a STAT echocardiogram which reveals a severely dilated right ventricle with poor function, indicative of worsening pulmonary hypertension. In addition, the echocardiogram shows an increased left-to-right shunt, suggestive of the progression of the ventricular septal defect. Laboratory results reveal an increase in B-type natriuretic peptide (BNP) to 1,500 pg/mL, reflecting worsening heart failure. Blood gas analysis shows a PaO2 of 55 mmHg and PaCO2 of 50 mmHg, confirming the patient's respiratory distress.

These findings suggest the patient's condition is rapidly deteriorating and he is developing congestive heart failure. The nurse must quickly communicate these results to the healthcare team and help prepare for emergent medical intervention. The next steps may include an increase in diuretic therapy, the initiation of inotropic support to improve cardiac function, and the consideration for mechanical ventilation to aid in respiratory distress. This case emphasizes the critical role of the nurse in monitoring, recognizing, and responding to signs of clinical deterioration in complex pediatric patients.

Section 3

New Complications:

Over the next several hours, the patient's condition continues to deteriorate. Despite the increased diuretic therapy, his edema worsens, and his urine output decreases to less than 1 mL/kg/hr, suggesting worsening renal function. Furthermore, the patient develops a fever of 38.5°C, and blood cultures confirm the presence of a gram-negative bacteremia, likely secondary to the use of invasive lines.

Response to Interventions:

Upon recognizing these new complications, the nurse immediately notifies the healthcare team. The patient is started on broad-spectrum antibiotics to combat the bacteremia. In addition, in response to the decreased urine output, the healthcare team orders a renal ultrasound, which shows signs of acute tubular necrosis, likely secondary to decreased perfusion from the worsening heart failure. The team initiates inotropic support with dobutamine and milrinone to improve cardiac output and renal perfusion. The nurse closely monitors the patient's hemodynamic status, urine output, and response to the inotropic agents.

These new complications and interventions create a critical juncture in the patient's journey. The nurse must continue to closely monitor the patient's status, recognizing and communicating any changes to the healthcare team. The focus now shifts to managing the patient's heart failure and potential renal failure, as well as the systemic infection.

Section 4

Change in Patient Status:

Over the next 24 hours, the patient’s condition continues to decline. He becomes increasingly lethargic and his respiratory rate increases to 36 breaths per minute, likely due to the worsening heart failure and fluid overload. His blood pressure is noted to be 85/50 mmHg and heart rate has risen to 120 beats per minute, indicating a compensatory response to decreased cardiac output. Additionally, the patient's oxygen saturation drops to 88% on room air, and he exhibits signs of increased work of breathing including nasal flaring and intercostal retractions.

Response to Interventions:

Upon recognizing these changes, the nurse immediately informs the healthcare team and supplemental oxygen is administered via nasal cannula, which helps to improve the oxygen saturation to 92%. The healthcare team also orders a chest X-ray, which shows signs of pulmonary edema, likely secondary to the worsening heart failure. The team decides to start the patient on bi-level positive airway pressure (BiPAP) to assist with his breathing and to help alleviate the pulmonary edema. The nurse closely monitors the patient's respiratory status, vital signs, and response to the BiPAP therapy. The team also increases the dose of the inotropic agents in an attempt to improve the patient's cardiac output and blood pressure. The nurse must continue to closely monitor the patient's status, recognizing and communicating any changes to the healthcare team, with the aim of preventing further deterioration.

Section 5

New Diagnostic Results:

Following the adjustment of the inotropic agents, the nurse draws blood samples for laboratory investigations. The complete blood count shows a rise in the white blood cell count to 18,000 cells/microliter, suggestive of a potential infection. The patient's arterial blood gas (ABG) results show a pH of 7.28, PaCO2 of 55 mmHg, and HCO3 of 24 mEq/L, indicating respiratory acidosis. These findings are consistent with the patient's increased work of breathing and the worsening heart failure. In addition, the patient’s serum B-type natriuretic peptide (BNP) has increased to 1500 pg/mL, further indicating worsening heart failure. The serum electrolytes show hyponatremia (Na+ 130 mEq/L) and hyperkalemia (K+ 5.6 mEq/L), likely secondary to the increased doses of inotropic agents.

Response to Interventions:

With the new lab results, the nurse promptly informs the healthcare team of the changes. The team decides to commence intravenous antibiotics to combat the suspected infection and to adjust the inotropic agents due to the electrolyte imbalances. The BiPAP settings are also adjusted to better manage the respiratory acidosis. The nurse continues to closely monitor the patient, paying particular attention to changes in respiratory status, vital signs, and signs of infection. The nurse also ensures regular follow-up lab investigations to monitor the effectiveness of interventions and to detect any further changes early. Despite the challenges, the nurse remains vigilant and proactive in managing this complex patient, keeping the healthcare team informed of all developments.