A patient receiving thrombolytic therapy for acute myocardial infarction has rapidly deteriorated, showing signs of cardiogenic shock and respiratory failure. After initiating norepinephrine and preparing for intubation, what is the most critical next step for the nurse to prioritize in managing this patient's evolving condition?

C) Monitor for signs of bleeding complications associated with thrombolytic therapy.

A) Increase the rate of norepinephrine infusion to improve perfusion.

B) Prepare for the administration of intravenous fluids to correct hypotension.

C) Monitor for signs of bleeding complications associated with thrombolytic therapy.

D) Arrange for an urgent repeat echocardiogram to assess cardiac function.

A patient undergoing thrombolytic therapy for a myocardial infarction has developed signs of cardiogenic shock and severe respiratory distress. The healthcare team has initiated norepinephrine to stabilize blood pressure and is preparing for intubation. As the nurse, which of the following interventions is the highest priority to ensure patient safety and optimize outcomes during this critical period?

D) Coordinate with the respiratory therapist to ensure adequate preoxygenation before intubation

A) Administer a sedative prior to intubation to prevent anxiety and agitation

B) Monitor for signs of bleeding due to thrombolytic therapy and prepare to administer reversal agents if necessary

C) Increase the norepinephrine infusion rate to rapidly elevate blood pressure

D) Coordinate with the respiratory therapist to ensure adequate preoxygenation before intubation

A patient with a large saddle pulmonary embolism and right ventricular strain is experiencing a drop in hemoglobin levels and elevated lactate levels. Which nursing intervention is most appropriate to prioritize at this time?

A) Administer additional thrombolytic therapy to dissolve the embolism.

C) Increase IV fluid administration to optimize preload and support cardiac output.

D) Prepare the patient for emergent surgical embolectomy to remove the obstruction.

A patient with a large saddle pulmonary embolism and significant right ventricular strain has developed a marked decrease in hemoglobin levels and elevated lactate levels following thrombolytic therapy. Given the current clinical data, which of the following interventions should the nurse anticipate as the priority in collaboration with the healthcare team?

D) Implement continuous echocardiographic monitoring and adjust fluid management to optimize right ventricular preload without exacerbating heart failure.

A) Initiate an immediate transfusion of packed red blood cells to address the anemia and improve oxygen delivery.

B) Discontinue thrombolytic therapy and prepare the patient for emergent surgical embolectomy due to the risk of bleeding complications.

C) Administer intravenous fluids aggressively to counteract hypoperfusion and improve hemodynamic stability.

D) Implement continuous echocardiographic monitoring and adjust fluid management to optimize right ventricular preload without exacerbating heart failure.

A patient with a large saddle pulmonary embolism is experiencing acute worsening respiratory distress and signs of cardiogenic shock despite ongoing thrombolytic therapy and vasopressor support. Given the current clinical scenario, what is the most appropriate immediate nursing action to support the patient's deteriorating condition?

C) Initiate extracorporeal membrane oxygenation (ECMO) to stabilize respiratory and circulatory function.

A) Increase the rate of thrombolytic infusion to expedite clot resolution.

B) Prepare the patient for emergent embolectomy by coordinating with the surgical team.

C) Initiate extracorporeal membrane oxygenation (ECMO) to stabilize respiratory and circulatory function.

D) Administer additional vasopressors to improve blood pressure and cardiac output.

A patient with a large saddle pulmonary embolism is experiencing acute worsening respiratory distress, hemodynamic instability, and signs of progressing cardiogenic shock despite ongoing thrombolytic therapy and vasopressor support. As the nurse on the team, what is the most appropriate immediate action to stabilize the patient?

B) Recommend initiation of extracorporeal membrane oxygenation (ECMO) immediately.

A) Increase the dose of vasopressors to improve blood pressure.

B) Recommend initiation of extracorporeal membrane oxygenation (ECMO) immediately.

C) Administer a bolus of intravenous fluids to increase cardiac preload.

D) Prepare the patient for immediate transfer to the operating room for surgical embolectomy.

A patient with a massive pulmonary embolism is on veno-arterial extracorporeal membrane oxygenation (VA-ECMO) and is being prepared for pulmonary embolectomy. As the nurse, which intervention should be prioritized to prevent potential complications associated with ECMO therapy?

B) Monitoring for signs of bleeding and managing anticoagulation levels

A) Administering continuous heparin infusion to prevent thromboembolic events

B) Monitoring for signs of bleeding and managing anticoagulation levels

C) Ensuring adequate sedation to prevent patient movement and cannula dislodgement

D) Regularly assessing neurological status to detect signs of cerebral hypoxia

A patient undergoing veno-arterial extracorporeal membrane oxygenation (VA-ECMO) for support due to severe pulmonary embolism is showing signs of improving oxygenation and perfusion. However, the nursing team must remain vigilant for complications. Which of the following assessments should the nurse prioritize to detect early signs of a common ECMO complication?

C) Assessing for signs of bleeding by observing insertion sites and measuring hemoglobin levels.

A) Monitoring for signs of hemolysis by checking urine color and laboratory hemoglobin levels.

B) Evaluating neurological status frequently to detect any changes in consciousness.

C) Assessing for signs of bleeding by observing insertion sites and measuring hemoglobin levels.

D) Checking for signs of infection by monitoring temperature and white blood cell count.

Pulmonary embolism - Nursing Case Study

Pathophysiology

• Primary mechanism: Venous thromboembolism, typically originating from deep vein thrombosis (DVT), travels through circulation and lodges in pulmonary arteries, causing obstruction. This impedes blood flow, leading to increased pulmonary vascular resistance and impaired gas exchange.

• Secondary mechanism: The obstruction triggers release of inflammatory mediators, causing vasoconstriction and bronchoconstriction, exacerbating ventilation-perfusion mismatch and hypoxemia.

• Key complication: Acute right ventricular (RV) dysfunction occurs due to increased afterload from the obstructed pulmonary circulation, potentially leading to RV failure, systemic hypotension, and cardiogenic shock if untreated.

Patient Profile

Demographics:

65-year-old male, retired miner

History:

• Key past medical history: Deep vein thrombosis, hypertension, chronic obstructive pulmonary disease (COPD)

• Current medications: Warfarin, Lisinopril, Albuterol inhaler

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Sudden onset of severe chest pain and difficulty breathing

• Key symptoms: Shortness of breath, rapid heart rate, dizziness, coughing up blood, cyanosis of lips and fingertips

• Vital signs: Blood pressure 88/56 mmHg, heart rate 132 bpm, respiratory rate 28 breaths per minute, oxygen saturation 82% on room air, temperature 37.2°C (99°F)

Section 1

As the healthcare team initiates an emergency response, the initial assessment reveals further critical findings. Upon auscultation, diminished breath sounds are noted in the lower lung fields, accompanied by fine crackles that suggest fluid accumulation. The patient exhibits significant jugular venous distension, indicative of elevated central venous pressure and potential right heart strain. Peripheral edema is also present, raising concerns about deteriorating cardiac function. A rapid bedside echocardiogram confirms acute right ventricular dilation and hypokinesis, suggesting severe RV dysfunction. Despite supplemental oxygen, the patient's oxygen saturation remains critically low at 85% on a non-rebreather mask, necessitating consideration of advanced airway management.

Laboratory results further complicate the clinical picture. A complete blood count reveals leukocytosis, hinting at an inflammatory response. Arterial blood gas analysis indicates severe hypoxemia with a pH of 7.28, PaCO2 of 58 mmHg, and HCO3- of 24 mEq/L, revealing a mixed respiratory and metabolic acidosis. Elevated D-dimer levels corroborate the likelihood of significant thromboembolic activity. Additionally, troponin levels are elevated, suggesting myocardial injury secondary to strain, while a BNP level of 800 pg/mL points towards cardiac stress. These findings, combined with the patient's hemodynamic instability, signal impending cardiogenic shock.

The patient's condition demands immediate intervention with thrombolytic therapy and consideration of vasopressor support to stabilize blood pressure. However, the administration of anticoagulation in the context of hypoperfusion and potential bleeding risks, such as hemoptysis, requires careful deliberation. The team must weigh the risks and benefits of escalating anticoagulation while preparing for potential mechanical ventilation to address worsening respiratory failure. As the situation unfolds, continuous monitoring and dynamic reassessment are crucial to navigate the complex interplay of pulmonary, cardiac, and systemic factors at play.

Section 2

As the healthcare team navigates the critical complexities of the patient's condition, a change in patient status emerges that demands urgent attention. Despite the initiation of thrombolytic therapy, the patient's hemodynamic status deteriorates rapidly. The blood pressure plummets to 80/50 mmHg, and heart rate escalates to 130 beats per minute, indicating progression towards cardiogenic shock. The skin becomes cool and clammy, and capillary refill time exceeds five seconds, reflecting systemic hypoperfusion. Additionally, altered mental status is observed, with the patient becoming increasingly confused and disoriented, highlighting the urgency of cerebral hypoxia.

Amidst this clinical decline, a repeat arterial blood gas analysis shows worsening hypoxemia, with an oxygen saturation now at 78% despite high-flow oxygen therapy. The pH has further dropped to 7.22, with PaCO2 rising to 62 mmHg, and HCO3- remaining unchanged at 24 mEq/L, underscoring the compounded respiratory and metabolic acidosis. These alarming developments necessitate immediate intervention. The decision is made to initiate vasopressor support with norepinephrine to maintain perfusion and stabilize blood pressure, while preparations for intubation and mechanical ventilation are expedited to manage the escalating respiratory failure.

As the team works swiftly to address these new complications, attention turns to the potential for further thromboembolic events and the risk of bleeding associated with thrombolytic therapy. Continuous monitoring is essential, with serial echocardiograms and coagulation profiles guiding the ongoing therapeutic approach. The interplay of pulmonary, cardiac, and systemic factors remains a delicate balance, demanding advanced clinical reasoning to anticipate and mitigate additional challenges that may arise. The evolving situation highlights the need for ongoing reassessment and adaptation of the treatment plan to navigate the intricate path of this patient's journey.

Section 3

Amid the urgent interventions, the healthcare team receives new diagnostic results that further complicate the patient's clinical picture. A CT pulmonary angiogram reveals a large saddle pulmonary embolism with significant right ventricular strain, as evidenced by a markedly dilated right ventricle and septal bowing. This finding confirms the extent of the obstruction and the strain on the heart, explaining the patient's rapid hemodynamic decline. Concurrently, laboratory tests reveal a significant drop in hemoglobin levels, now at 8.5 g/dL, suggesting potential bleeding complications from the thrombolytic therapy, which further complicates the management strategy. Additionally, elevated lactate levels at 5.8 mmol/L indicate severe tissue hypoperfusion and ongoing metabolic distress.

These results necessitate a reevaluation of the risk-benefit balance of continuing thrombolytic therapy amidst the risk of hemorrhage. The team must consider the initiation of a transfusion protocol to address the anemia and support oxygen-carrying capacity, while simultaneously managing the risk of further embolic events. Continuous echocardiographic monitoring reveals a decrease in right ventricular function, requiring close attention to fluid management to optimize preload without exacerbating right heart failure. The potential for emergent surgical intervention, such as embolectomy, is weighed against the patient's current instability and bleeding risk.

The complexity of the case demands heightened vigilance for signs of further deterioration or improvement in response to interventions. The multidisciplinary team, including cardiology, pulmonology, and critical care specialists, collaborates closely to tailor the evolving treatment plan. The patient's condition remains precarious, with each decision carrying significant implications for outcomes. The situation underscores the importance of integrating new data promptly, reassessing therapeutic priorities, and maintaining a dynamic approach to patient care. As the team navigates these challenges, they prepare for potential next steps, including advanced cardiac support and surgical consultation, poised to act swiftly as the patient's journey unfolds.

Section 4

As the healthcare team continues to manage the complex case of the patient with a large saddle pulmonary embolism, new complications emerge, demanding immediate attention and further clinical reasoning. Despite initial interventions and the cautious continuation of thrombolytic therapy, the patient's condition takes a sudden turn when he develops signs of acute worsening respiratory distress. His respiratory rate escalates to 38 breaths per minute with accessory muscle use, and oxygen saturation drops precipitously to 84% on high-flow oxygen therapy, indicating severe hypoxemia. Arterial blood gases reveal a pH of 7.25, PaCO2 of 58 mmHg, and PaO2 of 52 mmHg, confirming a respiratory acidosis with severe hypoxemia.

A repeat bedside echocardiogram shows no significant improvement in right ventricular function, with continued septal bowing and decreased cardiac output. Concurrently, the patient's blood pressure plummets to 82/48 mmHg, and heart rate remains elevated at 128 bpm, despite previous vasopressor support. The combination of hemodynamic instability and respiratory compromise suggests a progression towards cardiogenic shock, exacerbated by ongoing right ventricular failure and possibly compounded by a worsening pulmonary embolic burden.

These developments necessitate an urgent reevaluation of the treatment strategy. The team contemplates the immediate escalation to advanced cardiac support, such as extracorporeal membrane oxygenation (ECMO), to stabilize the patient's respiratory and circulatory systems while considering the feasibility of surgical intervention. A multidisciplinary discussion emphasizes the need for rapid coordination with cardiothoracic surgery for potential emergent embolectomy. The patient's precarious state underscores the critical need for timely and decisive action, as the team prepares to implement these high-risk, high-reward interventions in hopes of altering the trajectory of this life-threatening crisis.

Section 5

As the team prepares to implement advanced cardiac support, a sudden change in the patient’s status demands immediate attention. The patient's level of consciousness diminishes rapidly, with a Glasgow Coma Scale score dropping to 8, indicating a significant decline in neurological function. Simultaneously, the patient's skin becomes mottled, and peripheral pulses are barely palpable, suggesting a critical reduction in peripheral perfusion. A quick reassessment reveals that the patient's oxygen saturation has further deteriorated to 78% despite maximal non-invasive support, while his blood pressure continues to nosedive to 76/44 mmHg.

Recognizing the urgent need for enhanced hemodynamic and respiratory support, the decision is made to initiate veno-arterial extracorporeal membrane oxygenation (VA-ECMO). The ECMO team rapidly mobilizes, and cannulation is performed at the bedside under ultrasound guidance, with the patient sedated and intubated for airway protection. As ECMO flow is established, there is a noticeable improvement in oxygenation and perfusion parameters; oxygen saturation climbs to 92%, and mean arterial pressure stabilizes at 65 mmHg with reduced reliance on vasopressors. Despite these initial gains, the team remains vigilant, aware of the potential complications associated with ECMO, including bleeding and thromboembolic events.

Parallelly, new diagnostic results from a CT pulmonary angiogram reveal an increased clot burden, confirming the need for surgical intervention. The imaging shows extensive bilateral pulmonary artery occlusions extending into segmental branches, with a significant thrombus load in the left main pulmonary artery. This finding corroborates the need for an emergent pulmonary embolectomy, as conservative measures alone appear insufficient to resolve the embolic burden. With ECMO providing temporary stabilization, the patient is prepped for urgent transfer to the operating room, where the surgical team stands ready to perform the life-saving procedure. The multidisciplinary team remains cautiously optimistic, understanding the gravity of the patient's condition and the challenges that lie ahead.