pulmonary embolism - Nursing Case Study

Pathophysiology

• Primary mechanism: A pulmonary embolism (PE) occurs when a blood clot, usually from the deep veins of the legs (deep vein thrombosis), travels to the lungs and lodges in the pulmonary arteries, obstructing blood flow and impairing oxygen exchange.

• Secondary mechanism: The obstruction causes increased pressure in the right side of the heart (right ventricular strain), which can lead to decreased cardiac output and potential right heart failure due to the heart's inability to effectively pump blood against the increased resistance.

• Key complication: The impaired oxygenation and potential heart failure can lead to hypoxemia and systemic hypotension, which, if untreated, may result in shock or death. Prompt recognition and treatment are crucial to prevent serious outcomes.

Patient Profile

Demographics:

45-year-old female, office manager

History:

• Key past medical history: Hypertension, deep vein thrombosis (DVT) two years ago

• Current medications: Lisinopril 10 mg daily, Warfarin 5 mg daily

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Sudden onset of shortness of breath and chest pain

• Key symptoms: Dyspnea, pleuritic chest pain, slight hemoptysis, mild anxiety

• Vital signs: Blood pressure 140/90 mmHg, heart rate 110 bpm, respiratory rate 24 breaths per minute, temperature 98.6°F, oxygen saturation 88% on room air

Section 1

As the patient continues to be monitored in the emergency department, her oxygen saturation remains low despite supplemental oxygen therapy via nasal cannula. Her respiratory rate increases to 28 breaths per minute, and she exhibits increased use of accessory muscles, indicating worsening respiratory distress. A repeat set of vital signs shows a blood pressure of 130/85 mmHg, heart rate of 115 bpm, and her oxygen saturation is now 90% on 3L of oxygen. An arterial blood gas (ABG) analysis reveals a pH of 7.47, PaCO2 of 33 mmHg, and PaO2 of 58 mmHg, indicating respiratory alkalosis with significant hypoxemia.

A CT pulmonary angiogram is performed, confirming the presence of multiple emboli in the right and left pulmonary arteries, with signs of right ventricular dilation. This finding is consistent with right heart strain. Given the patient's history of DVT and current anticoagulation therapy with Warfarin, her INR is checked and noted to be subtherapeutic at 1.8, which may have contributed to the recurrence of thromboembolism. The clinical team discusses the need for immediate anticoagulation adjustment to manage the acute PE and considers the potential for thrombolytic therapy if the patient's condition does not stabilize.

The patient begins to experience new onset of mild confusion and tachycardia, with her heart rate climbing to 130 bpm. These changes suggest a possible decrease in cerebral perfusion secondary to hypoxemia and may indicate the development of acute right heart failure. The clinical team must now prioritize interventions to stabilize her hemodynamics and improve oxygenation, balancing the risks of increased anticoagulation against the potential for bleeding complications. Close monitoring in an intensive care setting is warranted as her condition evolves, with the aim of preventing further deterioration and addressing the underlying pathophysiology of the pulmonary embolism.

Section 2

As the patient's condition continues to be monitored in the intensive care unit, her respiratory distress persists, and her mental status fluctuates between confusion and restlessness. A repeat ABG shows a worsening hypoxemia with a PaO2 of 54 mmHg, despite increasing supplemental oxygen to 6L via a non-rebreather mask. Her PaCO2 has decreased further to 30 mmHg, reflecting increased respiratory effort and persistent respiratory alkalosis. The patient's heart rate remains elevated at 128 bpm, and her blood pressure has dropped slightly to 125/80 mmHg. These findings suggest ongoing right ventricular strain and insufficient oxygenation, raising concerns about the adequacy of current interventions.

In response to these developments, the clinical team decides to initiate heparin therapy intravenously to achieve rapid anticoagulation, transitioning from her subtherapeutic Warfarin regimen. Despite the anticoagulation initiation, the patient develops new signs of hemodynamic instability, including jugular venous distension and a new S3 heart sound, indicative of worsening right-sided heart failure. The chest X-ray reveals an increase in pulmonary vascular congestion, suggesting that the heart's ability to compensate is diminishing, likely due to increased pulmonary artery pressures and ongoing strain.

Given these new complications, the team discusses the potential need for more aggressive intervention, such as thrombolytic therapy, to address the significant embolic burden and right heart strain. However, they must balance this decision with the risk of bleeding, particularly in light of anticoagulation therapy adjustments. The patient is closely monitored for signs of further deterioration, while the clinical team prepares to escalate care if necessary, including the possibility of mechanical ventilation support or surgical intervention if her condition does not improve. This critical juncture emphasizes the importance of reassessing the patient's response to treatment and making timely adjustments based on evolving clinical data.

Section 3

As the clinical team continues to monitor the patient, her condition takes a concerning turn. Despite initiating heparin therapy, her respiratory distress remains severe, and she becomes increasingly lethargic, with periods of unresponsiveness. Her vital signs indicate further deterioration, with her heart rate spiking to 140 bpm and blood pressure now dropping to 110/70 mmHg, raising alarms about her hemodynamic stability. The patient's oxygen saturation has decreased to 85% on the non-rebreather mask, prompting the team to consider escalating respiratory support.

A repeat echocardiogram is performed to assess the extent of right ventricular dysfunction. The results reveal significant right ventricular dilation and decreased right ventricular ejection fraction, with estimated pulmonary artery pressures markedly elevated, confirming severe pulmonary hypertension. These findings suggest that despite anticoagulation therapy, the embolic burden remains substantial, and the right heart is struggling to manage the increased pressure load.

Given the patient's worsening status and the echocardiographic evidence of severe right heart strain, the clinical team discusses the immediate need for thrombolytic therapy as a more aggressive approach to resolve the embolus. However, they remain cautious about the bleeding risks associated with such treatment, especially with the recent adjustment to anticoagulation. As they deliberate, the patient's hypoxemia and hemodynamic instability reinforce the urgency for intervention. The team decides to consult a cardiothoracic specialist to evaluate the feasibility of surgical embolectomy as an alternative, preparing for possible transfer to a tertiary care center if necessary. This decision underscores the complexity of managing acute pulmonary embolism with right heart failure and the critical need for timely, multidisciplinary collaboration to optimize patient outcomes.

Section 4

As the clinical team prepares for potential surgical intervention, they continue to closely monitor the patient’s status. During the next assessment, the nurse notes that the patient is becoming increasingly diaphoretic and her skin is cool and clammy to the touch, indicating further compromise in her circulatory system. Her heart rate remains elevated at 145 bpm, and her blood pressure has decreased further to 100/65 mmHg, signaling worsening hemodynamic instability. The patient's respiratory rate has increased to 30 breaths per minute, but her oxygen saturation struggles to maintain 83% despite the high-flow oxygen. These changes suggest a progression towards shock, likely due to the failing right heart impacting systemic circulation.

In light of these developments, the team decides to perform an urgent arterial blood gas (ABG) analysis to assess the extent of her respiratory and metabolic derangements. The ABG results reveal significant hypoxemia with a PaO2 of 55 mmHg, and a mixed respiratory and metabolic acidosis, evidenced by a pH of 7.25, PaCO2 of 50 mmHg, and HCO3- of 18 mEq/L. This combination of findings illustrates the profound impact of the pulmonary embolism on her respiratory function and the beginning of end-organ dysfunction due to poor perfusion.

With the patient's condition rapidly declining, the team underscores the need for immediate intervention. As they await the cardiothoracic specialist's input, they begin to discuss the logistics of initiating thrombolytic therapy in conjunction with potential mechanical ventilation to support her failing respiratory system. The complexity of managing the bleeding risks associated with thrombolytics, alongside the need for rapid oxygenation improvement, presents a challenging situation that requires careful balancing of risks and benefits to stabilize the patient. These critical decisions will shape the next steps in her treatment journey and highlight the importance of dynamic, evidence-based clinical reasoning in managing complex cases of pulmonary embolism with right heart failure.

Section 5

As the team initiates thrombolytic therapy and prepares for potential mechanical ventilation, they monitor the patient's response closely, recognizing the delicate balance required to optimize oxygenation while minimizing bleeding risks. Within the first hour of administering the thrombolytics, the patient's vital signs begin to show subtle improvements. Her heart rate decreases to 130 bpm, and her blood pressure stabilizes at 105/70 mmHg, suggesting a slight improvement in hemodynamic stability. However, her oxygen saturation remains critically low at 85%, and her respiratory rate continues to hover around 28 breaths per minute.

Despite these slight improvements, new complications arise. The patient begins to exhibit signs of altered mental status, becoming increasingly lethargic and less responsive to verbal stimuli. A repeat arterial blood gas analysis reveals some improvement in oxygenation with a PaO2 of 60 mmHg, yet the acidosis persists with a pH of 7.28, PaCO2 of 48 mmHg, and HCO3- of 19 mEq/L. These findings suggest ongoing respiratory insufficiency despite high-flow oxygen and indicate potential cerebral hypoxia, necessitating urgent intervention.

In response to the deteriorating neurological status and persistent hypoxemia, the team decides to proceed with mechanical ventilation. This decision is not taken lightly, given the associated risks, but it is deemed necessary to ensure adequate ventilation and oxygenation. The nursing team prepares for intubation, while the medical team continues to assess for any bleeding complications from the thrombolytics. As the patient is intubated, the clinical team remains vigilant, aware that their actions in the next few hours will be critical in determining the trajectory of her recovery. The unfolding scenario underscores the need for ongoing assessment and adaptation in the face of rapidly changing clinical conditions.