pulmonary embolism - Nursing Case Study
Pathophysiology
• Primary mechanism: A pulmonary embolism (PE) occurs when a blood clot, often originating from deep veins in the legs (deep vein thrombosis), travels through the bloodstream and lodges in the pulmonary arteries, blocking blood flow to lung tissue.
• Secondary mechanism: The obstruction of blood flow causes increased pressure in the pulmonary arteries (pulmonary hypertension) and impairs oxygen exchange, leading to decreased oxygen levels in the blood and potential strain on the right side of the heart.
• Key complication: Reduced oxygenation and increased cardiac workload can result in acute respiratory distress and right ventricular failure, emphasizing the need for rapid diagnosis and treatment to prevent significant morbidity and mortality.
Patient Profile
Demographics:
45-year-old female, office manager
History:
• Key past medical history: Deep vein thrombosis (DVT) 3 years ago, hypertension
• Current medications: Warfarin, Lisinopril
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Sudden onset shortness of breath
• Key symptoms: Chest pain, cough with mild hemoptysis, lightheadedness
• Vital signs: Blood pressure 95/60 mmHg, heart rate 110 bpm, respiratory rate 28 breaths per minute, oxygen saturation 88% on room air, temperature 37.2°C
Section 1
As the emergency department team continues to evaluate the patient, the initial assessment findings are critical in guiding the next steps. Upon physical examination, the patient appears anxious and is using accessory muscles to breathe. Her skin is slightly diaphoretic and cool to the touch, indicating potential inadequate perfusion. Auscultation of the lungs reveals diminished breath sounds bilaterally with occasional crackles, particularly in the right lung base. Cardiac examination shows tachycardia, and a pronounced jugular venous distension is noted, suggesting increased venous pressure. Peripheral edema is absent, but the patient reports mild calf tenderness, raising suspicion of a possible recurrent DVT as the source of the embolism.
Lab results return with a significantly elevated D-dimer level, consistent with the presence of a thrombotic event. Arterial blood gas analysis indicates respiratory alkalosis with a pH of 7.48, PaCO2 of 32 mmHg, and PaO2 of 60 mmHg, confirming hypoxemia and compensatory hyperventilation. An urgent CT pulmonary angiogram is ordered, revealing a large embolus in the right main pulmonary artery, confirming the diagnosis of a substantial pulmonary embolism. Additionally, the echocardiogram shows signs of right ventricular strain, further suggesting increased pressure in the pulmonary circuit.
These findings prompt immediate initiation of anticoagulation therapy with heparin to prevent further clot propagation and to stabilize the patient's condition. Oxygen therapy is started, and the patient is closely monitored in a high-acuity setting to assess her response to treatment and to watch for any additional complications, such as worsening hypoxemia or signs of right heart failure. The healthcare team prepares for potential escalations in care, including the consideration of thrombolytic therapy or surgical intervention if the patient's condition deteriorates.
Section 2
As the patient is monitored in the high-acuity setting, the healthcare team notices a change in her status that raises concern. Over the next few hours, the patient begins to exhibit increased respiratory distress. Her respiratory rate escalates to 34 breaths per minute, and she becomes increasingly tachycardic, with her heart rate rising to 130 beats per minute. The oxygen saturation, despite supplemental oxygen, drops to 88%, indicating worsening hypoxemia. The patient also complains of new-onset chest pain, which she describes as sharp and pleuritic in nature, exacerbated by deep inspiration.
In response to these developments, the team re-assesses her cardiovascular status and discovers a drop in blood pressure to 90/60 mmHg, suggesting potential hemodynamic instability. Repeat auscultation of the lungs reveals more pronounced crackles at the right lung base. The chest pain and hypoxemia, coupled with hypotension, are suggestive of a possible extension of the pulmonary embolism or the development of a new complication, such as pulmonary infarction or worsening right ventricular dysfunction.
Given these changes, an urgent repeat echocardiogram is performed, revealing further deterioration in right ventricular function, with evidence of increased right ventricular dilation and decreased contractility, consistent with impending right heart failure. The clinical team must now deliberate on the next steps, considering the initiation of thrombolytic therapy despite the risks, given the signs of hemodynamic compromise and the potential for rapid deterioration. This decision requires careful clinical reasoning, weighing the benefits of aggressive intervention against the potential for bleeding complications, and underscores the need for continuous monitoring and timely decision-making in the management of complex pulmonary embolism cases.
Section 3
As the healthcare team deliberates on the next steps, they decide to initiate thrombolytic therapy to address the possible extension of the pulmonary embolism and the associated hemodynamic compromise. Given the critical situation, they administer tissue plasminogen activator (tPA) with close monitoring for any adverse effects. Over the next hour, the patient's respiratory rate begins to stabilize, dropping to 28 breaths per minute, and her heart rate decreases slightly to 120 beats per minute. However, her oxygen saturation remains at a concerning level of 90%, and she continues to report chest pain, though slightly diminished in intensity.
Concurrently, new diagnostic results from a repeat CT pulmonary angiogram reveal an increase in the size of the embolus in the right pulmonary artery, confirming the suspicion of embolic extension. Laboratory tests show a drop in hemoglobin to 10 g/dL, raising concerns about potential bleeding complications from the thrombolytic therapy. The patient's coagulation profile is closely monitored, with results indicating an international normalized ratio (INR) of 1.6 and activated partial thromboplastin time (aPTT) within therapeutic range, suggesting that the bleeding risk, while present, is not yet critical.
Despite the partial improvement, the patient suddenly experiences worsening dyspnea and increased chest discomfort, accompanied by a further drop in blood pressure to 85/55 mmHg. These changes prompt the team to consider additional complications, such as worsening right heart failure or a new thrombotic event. The need for continuous hemodynamic support becomes apparent, and the team considers the initiation of vasopressor therapy to stabilize the patient's blood pressure while continuing to provide supplemental oxygen and monitor closely for any signs of bleeding or further hemodynamic deterioration. The situation underscores the complex interplay of therapeutic interventions and the vigilant assessment required to navigate the challenges of managing severe pulmonary embolism.
Section 4
The healthcare team decides to prioritize the initiation of vasopressor therapy to address the patient's hypotension, opting for norepinephrine to maintain adequate perfusion and stabilize blood pressure. As the norepinephrine infusion is started, the patient's blood pressure gradually increases to 95/60 mmHg, providing a slight improvement in hemodynamic stability. Despite this, her oxygen saturation remains borderline at 91%, and she continues to experience significant respiratory distress, with a respiratory rate now at 32 breaths per minute. The persistent chest pain, although somewhat relieved, raises concerns about ongoing cardiac strain.
To further evaluate her condition, the team orders an echocardiogram, which reveals signs of right ventricular dysfunction, consistent with strain from the pulmonary embolism. The echocardiogram shows mild right ventricular dilatation and moderate tricuspid regurgitation, indicating that the embolic burden is still causing significant hemodynamic compromise. Meanwhile, laboratory tests show a slight increase in D-dimer levels, reinforcing the suspicion of ongoing thrombotic activity. The team recognizes the need for a delicate balance in managing the risk of bleeding from thrombolytic therapy while also addressing the embolic extension.
Acknowledging the delicate situation, the healthcare team deliberates on the next steps, considering the potential need for surgical or interventional radiology consultation for further clot removal if the patient's condition does not improve. The priority remains to stabilize the patient while minimizing additional risks. The clinical reasoning process involves weighing the benefits of continuing aggressive anticoagulation and thrombolysis against the potential complications, as the patient's journey unfolds with cautious optimism and vigilant monitoring. This critical juncture underscores the importance of integrating diagnostic findings with therapeutic interventions to guide the patient's care trajectory effectively.
Section 5
As the healthcare team monitors the patient's response to the interventions, a new complication emerges. Despite the initial hemodynamic improvement with norepinephrine, the patient's respiratory status deteriorates further. Her oxygen saturation drops to 88% on high-flow oxygen, and her respiratory rate increases to 36 breaths per minute, indicating significant respiratory distress. Auscultation reveals diminished breath sounds on the right side and coarse crackles bilaterally, suggesting the development of atelectasis or possible pulmonary edema as a result of the ongoing hemodynamic compromise and right-sided heart strain.
In response to these alarming changes, the team orders a chest X-ray to assess the pulmonary status more comprehensively. The imaging reveals an enlargement of the right heart border, consistent with the echocardiogram findings of right ventricular dysfunction, and also shows diffuse patchy opacities in both lung fields. These findings raise the concern for pulmonary edema secondary to heart failure, possibly exacerbated by the high pulmonary artery pressures due to the embolism. In light of these developments, the team considers the judicious use of diuretics to manage fluid overload while carefully monitoring renal function given the patient's hemodynamic instability.
The clinical team now faces a critical decision-making juncture. While the patient remains at significant risk for further complications, such as cardiogenic shock or respiratory failure, the priority shifts to optimizing respiratory support and revisiting anticoagulation strategies. This includes re-evaluating the potential for advanced interventions such as catheter-directed thrombolysis or surgical embolectomy. The integrated approach requires balancing the immediate need to relieve right ventricular strain and improve oxygenation against the risks posed by invasive procedures. The healthcare team remains vigilant, employing a combination of clinical reasoning and interdisciplinary collaboration to navigate this complex clinical scenario.