pulmonary embolism - Nursing Case Study

Pathophysiology

• Primary mechanism: A pulmonary embolism 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. This obstructs blood flow to lung tissue, leading to decreased oxygen exchange and increased pressure in the pulmonary circulation.

• Secondary mechanism: The obstruction causes a sudden increase in pressure in the right side of the heart, as it struggles to push blood through the blocked vessels. This can lead to right ventricular strain and potentially heart failure if the clot burden is significant.

• Key complication: The reduced oxygenation and increased cardiac strain can result in hypoxemia and potentially life-threatening conditions such as shock or cardiac arrest if not promptly addressed.

Patient Profile

Demographics:

55-year-old male, construction worker

History:

• Key past medical history: Hypertension, Deep Vein Thrombosis (DVT) 2 years ago

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

• Allergies: Penicillin

Current Presentation:

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

• Key symptoms: Dyspnea, pleuritic chest pain, mild hemoptysis, lightheadedness

• Vital signs: Blood pressure 100/65 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 clinical team continues to assess the patient, a new set of diagnostic results provides further insight into his condition. A CT pulmonary angiography confirms the presence of a large embolus in the right pulmonary artery, consistent with a significant pulmonary embolism. Additionally, an echocardiogram reveals signs of right ventricular strain, indicating that the clot is placing considerable pressure on the right side of the heart. Blood tests show elevated D-dimer levels, which support the diagnosis of pulmonary embolism, and arterial blood gas analysis reveals a pH of 7.34, PaCO2 of 48 mmHg, and PaO2 of 60 mmHg, indicating respiratory acidosis and significant hypoxemia.

These findings prompt the healthcare team to initiate a more aggressive treatment plan. The patient is started on supplemental oxygen to improve his oxygen saturation levels, and intravenous fluids are administered cautiously to support blood pressure without exacerbating right ventricular overload. Heparin is initiated as a bridging anticoagulant therapy to enhance the effectiveness of warfarin and prevent further clot formation. Despite these interventions, the patient's oxygen saturation remains suboptimal, and his blood pressure begins to decrease further, indicating he may be developing shock.

In light of the patient's worsening hemodynamic status and persistent hypoxemia, the team must consider additional therapeutic options. Thrombolytic therapy is debated, weighing the risks of bleeding against the potential benefits of rapidly dissolving the clot to relieve the strain on the heart. This decision-making process requires careful clinical reasoning and collaboration among the healthcare providers, as they strive to stabilize the patient and prevent further complications.

Section 2

As the healthcare team continues to monitor the patient, they notice a change in his status that demands immediate attention. The patient's respiratory rate has increased to 32 breaths per minute, and he is exhibiting increased use of accessory muscles, suggesting worsening respiratory distress. His heart rate has climbed to 130 beats per minute, and his blood pressure has dropped to 85/50 mmHg, indicating a state of compensatory shock likely due to decreased cardiac output from the right ventricular strain. Despite oxygen therapy, his oxygen saturation remains at 88%, prompting concern about his ability to maintain adequate gas exchange.

The team conducts a reassessment and observes that the patient is becoming increasingly lethargic, with decreased responsiveness to verbal stimuli. This change in mental status, coupled with his unstable vital signs, suggests a progression towards cardiogenic shock. The team performs a bedside ultrasound, which confirms further right ventricular dilation and impaired contractility, highlighting the urgency of the situation.

Given the patient's declining condition, the healthcare team revisits the possibility of thrombolytic therapy. Balancing the risks of hemorrhage with the critical need to relieve the clot burden, they decide to proceed with thrombolysis as the potential benefits now outweigh the risks. The patient's deteriorating hemodynamic status and impending respiratory failure necessitate this aggressive intervention to rapidly restore pulmonary blood flow and stabilize the cardiovascular system. The team prepares to administer the thrombolytic agent, closely monitoring for any signs of bleeding while hoping for a favorable response to this high-stakes treatment strategy.

Section 3

In the hours following the administration of thrombolytic therapy, the healthcare team closely monitors the patient's response. Initially, there is a slight improvement in his respiratory function; his oxygen saturation increases to 92% with continued supplemental oxygen, and his respiratory rate decreases to 28 breaths per minute. However, his heart rate remains elevated at 125 beats per minute, and his blood pressure hovers around 90/55 mmHg, indicating ongoing hemodynamic instability. The team observes a modest increase in the patient's alertness, as he begins to respond more consistently to verbal stimuli, suggesting a slight improvement in his cerebral perfusion.

Laboratory results return, showing a decrease in D-dimer levels, providing indirect evidence that the clot burden may be reducing. However, repeat arterial blood gas analysis reveals a persistent metabolic acidosis with a pH of 7.31 and a bicarbonate level of 18 mmol/L, indicating that the patient's tissues are still under significant stress. Lactate levels remain elevated at 4 mmol/L, further confirming the presence of tissue hypoxia and inadequate perfusion.

Despite these encouraging signs, the team remains vigilant for potential complications of thrombolytic therapy, particularly bleeding. The patient develops a new onset of mild hematuria, raising concerns about bleeding risk. This complication necessitates a reassessment of the risk-benefit ratio of continuing aggressive anticoagulation. The team strategizes to manage any bleeding complications swiftly while maintaining focus on stabilizing the patient's hemodynamics. This delicate balance requires ongoing clinical reasoning as they aim to optimize the patient's recovery trajectory and prevent further deterioration.

Section 4

As the team monitors the patient's status, they notice a change in his vital signs and overall condition. Overnight, the patient's heart rate, which had been persistently elevated, begins to decrease, now registering at 110 beats per minute. However, his blood pressure remains low at 88/52 mmHg, suggesting persistent hemodynamic instability. The patient remains on supplemental oxygen, with his oxygen saturation stable at 92%. Despite the slight improvement in heart rate, the team is concerned about the ongoing hypotension and potential causes such as dehydration, hypovolemia, or continued right ventricular strain due to the pulmonary embolism.

In light of these findings, the healthcare team decides to conduct a repeat echocardiogram to assess the right ventricular function and look for signs of strain or failure. The echocardiogram reveals moderate right ventricular dilation and hypokinesis, confirming ongoing right heart strain. This finding suggests that despite thrombolytic therapy, the clot burden may still be significant, or the heart is struggling to cope with the imposed stress. Given the patient's hypotension and the echocardiogram results, the team considers the need for inotropic support to improve cardiac output and perfusion.

The patient also presents with a new complication: mild epigastric tenderness and a slight increase in abdominal girth. Concerned about potential gastrointestinal bleeding, the team orders a stool guaiac test and a complete blood count. The hemoglobin level returns marginally decreased at 11.2 g/dL from 12.5 g/dL, raising the suspicion of occult bleeding. The team must now weigh the risks of continuing anticoagulation against the potential for further bleeding, making adjustments to the treatment plan to address both the cardiovascular and bleeding complications while ensuring the patient's overall stability. This situation underscores the importance of ongoing clinical reasoning to navigate the complexities of thrombolytic therapy and its potential complications.

Section 5

As the team continues to monitor the patient, they note a change in his respiratory status. The patient begins to exhibit an increased respiratory rate, now at 28 breaths per minute, and reports feelings of increased shortness of breath and anxiety. The oxygen saturation has dropped slightly to 90% despite being on supplemental oxygen. These changes prompt the team to reassess his respiratory function and consider the possibility of worsening pulmonary status or other complications such as atelectasis or pleural effusion. The decision is made to perform a chest X-ray to further evaluate his respiratory condition.

The chest X-ray reveals mild bilateral pleural effusions and signs of atelectasis in the lower lobes, which may be contributing to the patient's increased work of breathing and hypoxemia. The team considers therapeutic options such as diuretics to manage the pleural effusions and aggressive pulmonary hygiene to address the atelectasis. Additionally, the possibility of using non-invasive ventilation to support his breathing is discussed to prevent further respiratory decline.

The healthcare team is now faced with the challenge of balancing the patient’s respiratory support with the ongoing need to manage his cardiovascular instability. Given the presence of pleural effusions and atelectasis, the team must employ clinical reasoning to adjust the treatment plan carefully, ensuring that any interventions do not exacerbate the existing right heart strain or risk further bleeding. This situation emphasizes the interconnectedness of the patient’s respiratory and cardiovascular systems and the need for a coordinated approach to manage these complex, evolving complications.