Mr. Thompson is receiving IV mannitol for cerebral edema following an ischemic stroke. Which assessment finding would indicate a therapeutic response to the treatment?

D) Decrease in intracranial pressure and improved level of consciousness

A) Blood pressure decreases to 110/70 mmHg

B) Decrease in right-sided weakness

C) Improvement in speech clarity

D) Decrease in intracranial pressure and improved level of consciousness

A nurse is caring for Mr. Thompson, who is experiencing an evolving ischemic stroke with complications including cerebral edema and decreased oxygen saturation. Which nursing intervention should be prioritized to address his current condition?

C) Start non-invasive ventilation support to improve oxygen saturation and reduce respiratory effort.

A) Administer a higher dose of IV mannitol to reduce cerebral edema immediately.

B) Increase the frequency of neurological assessments to monitor for changes in his condition.

C) Start non-invasive ventilation support to improve oxygen saturation and reduce respiratory effort.

D) Discontinue labetalol to avoid further reduction in blood pressure and ensure adequate cerebral perfusion.

A nurse is caring for Mr. Thompson, who is experiencing hypoventilation and decreased oxygen saturation despite receiving supplemental oxygen. After initiating BiPAP, what should the nurse prioritize in assessing to evaluate the effectiveness of this intervention?

B) Check Mr. Thompson's arterial blood gas (ABG) results to assess changes in PaCO2 and PaO2 levels.

A) Monitor Mr. Thompson's blood pressure to ensure it remains stable.

B) Check Mr. Thompson's arterial blood gas (ABG) results to assess changes in PaCO2 and PaO2 levels.

C) Observe for changes in Mr. Thompson's heart rate and rhythm.

D) Evaluate Mr. Thompson's Glasgow Coma Scale score to assess neurological status.

A nurse is caring for Mr. Thompson, whose respiratory status has deteriorated. Despite supplemental oxygen, his oxygen saturation remains low, and his breath sounds are diminished bilaterally. The team decides to initiate BiPAP therapy. What is the priority nursing action after initiating BiPAP for Mr. Thompson?

B) Reassess Mr. Thompson's level of consciousness and Glasgow Coma Scale score.

A) Monitor Mr. Thompson's blood pressure closely to assess for hypotension.

B) Reassess Mr. Thompson's level of consciousness and Glasgow Coma Scale score.

C) Check the BiPAP machine settings to ensure correct pressure levels.

D) Position Mr. Thompson in a high Fowler's position to facilitate breathing.

Mr. Thompson's condition includes a decrease in Glasgow Coma Scale to 8, elevated serum sodium, and diffuse cerebral edema. Which nursing intervention should take priority to potentially prevent further neurological deterioration?

B) Prepare for endotracheal intubation to secure the airway.

A) Administer additional hypertonic saline to manage intracranial pressure.

B) Prepare for endotracheal intubation to secure the airway.

C) Increase the frequency of neurological assessments to monitor changes.

D) Adjust the BiPAP settings to improve respiratory function.

Mr. Thompson is experiencing a decrease in his Glasgow Coma Scale and has elevated serum sodium levels. Which nursing intervention is most appropriate to address his current condition and prevent further complications?

B) Prepare for endotracheal intubation to secure the airway and protect neurological function

A) Increase the rate of hypertonic saline infusion to manage cerebral edema

B) Prepare for endotracheal intubation to secure the airway and protect neurological function

C) Administer a diuretic to reduce cerebral edema and lower serum sodium levels

D) Discontinue BiPAP and initiate continuous positive airway pressure (CPAP) to improve oxygenation

A nurse is caring for Mr. Thompson, who has developed frequent premature ventricular contractions (PVCs) due to mild hypokalemia after receiving hypertonic saline. Which of the following interventions should the nurse prioritize to address the underlying cause of the PVCs?

B) Begin potassium supplementation to correct the hypokalemia.

A) Administer a calcium supplement to stabilize cardiac function.

B) Begin potassium supplementation to correct the hypokalemia.

C) Increase the rate of hypertonic saline to correct sodium imbalance.

D) Administer a beta-blocker to reduce the frequency of PVCs.

A patient with frequent premature ventricular contractions (PVCs) due to mild hypokalemia is being managed with potassium supplementation. Which of the following nursing interventions is most critical in preventing further cardiac complications in this patient?

D) Assess the patient’s magnesium levels and supplement if necessary.

A) Monitor the patient’s serum potassium levels every 4 hours.

B) Encourage the patient to increase dietary potassium intake.

C) Administer potassium supplements with a full glass of water.

D) Assess the patient’s magnesium levels and supplement if necessary.

A nurse is caring for Mr. Thompson, who has developed increased intracranial pressure (ICP) following cardiac complications. After administering Mannitol and adjusting his care plan, which intervention should the nurse prioritize to ensure optimal patient outcomes?

A) Monitor serum electrolyte levels frequently.

B) Administer additional doses of Mannitol without physician order if ICP remains high.

C) Encourage early ambulation to promote circulation.

D) Lower the head of the bed to promote blood flow to the brain.

Mr. Thompson is exhibiting signs of increased intracranial pressure including pupillary changes, increased systolic blood pressure, and bradycardia. Which nursing intervention should be prioritized to help manage his intracranial pressure while ensuring cerebral perfusion?

B) Elevate the head of the bed to 30 degrees to promote venous drainage.

A) Administer a bolus of intravenous fluids to elevate blood pressure.

B) Elevate the head of the bed to 30 degrees to promote venous drainage.

C) Apply ice packs to the head to reduce brain metabolism.

D) Administer an antihypertensive medication to lower blood pressure.

Strok - Nursing Case Study

Pathophysiology

• Primary mechanism: Ischemic stroke occurs due to obstruction of cerebral blood flow, often from a thrombus or embolus, leading to decreased oxygen and nutrient supply, resulting in neuronal injury and death.

• Secondary mechanism: Hemorrhagic stroke involves the rupture of a cerebral blood vessel, causing bleeding in or around the brain, which increases intracranial pressure and further disrupts cerebral perfusion.

• Key complication: Both types can lead to cerebral edema, exacerbating brain tissue damage and potentially causing herniation or further neurological deficits.

Patient Profile

Demographics:

67-year-old male, retired civil engineer

History:

• Key past medical history: Hypertension, Type 2 Diabetes, Atrial Fibrillation

• Current medications: Lisinopril, Metformin, Warfarin, Atorvastatin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Sudden onset of right-sided weakness and speech difficulties

• Key symptoms: Right arm and leg weakness, slurred speech, facial droop on the right side, mild headache

• Vital signs: Blood pressure 170/95 mmHg, Heart rate 110 bpm (irregular), Respiratory rate 22 breaths per minute, Temperature 37.0°C, Oxygen saturation 92% on room air

Section 1

As the medical team continues to assess Mr. Thompson, further diagnostic imaging, notably a CT scan of the brain, reveals an evolving ischemic stroke in the distribution of the left middle cerebral artery. Additionally, laboratory results indicate an INR of 2.1, suggesting that his anticoagulation is within therapeutic range but still poses a risk for complications. The team notes slight worsening of his neurological deficits, with increased right-sided weakness and further deterioration in his speech, now characterized by expressive aphasia. These findings raise concerns about the potential development of cerebral edema, a common complication following an ischemic event, especially considering the patient's elevated blood pressure and history of atrial fibrillation.

In response to the situation, the healthcare team initiates a protocol to manage the risk of cerebral edema. Osmotherapy with IV mannitol is administered to reduce intracranial pressure, and his blood pressure is cautiously managed with intravenous labetalol, aiming to maintain cerebral perfusion without exacerbating the risk of hemorrhagic transformation. Despite these measures, a new complication arises as Mr. Thompson's oxygen saturation drops to 88% on room air, prompting the initiation of supplemental oxygen. The fluctuating oxygenation status suggests impaired respiratory effort, possibly due to brainstem involvement or decreased level of consciousness, necessitating close monitoring and potential escalation to non-invasive ventilation support.

This change in clinical status underscores the need for continuous reassessment and adaptation of the care plan. The team must now prioritize maintaining adequate cerebral perfusion while preventing further neurological compromise. As Mr. Thompson's condition evolves, the interplay of his underlying conditions, treatment interventions, and emerging complications will require careful consideration to achieve the best possible outcome. The next steps will involve close monitoring of his neurological status, frequent reassessment of his respiratory function, and timely adjustments to his therapeutic regimen.

Section 2

As the medical team continues to monitor Mr. Thompson, they observe a concerning change in his status. His respiratory effort becomes more labored, and his oxygen saturation fluctuates between 86% and 90% despite supplemental oxygen at 4 liters per minute via nasal cannula. His respirations are shallow at 28 breaths per minute, and auscultation of the lungs reveals diminished breath sounds bilaterally without any adventitious sounds, suggesting possible hypoventilation secondary to neurological impairment. His heart rate remains elevated at 102 beats per minute, and blood pressure is 165/92 mmHg. Neurological assessment reveals further deterioration in Mr. Thompson’s level of consciousness, now rated at a Glasgow Coma Scale of 10, with a noted decrease in response to verbal commands.

In light of these findings, the clinical team is compelled to reassess their management strategy, prioritizing the stabilization of Mr. Thompson’s respiratory function. A decision is made to escalate respiratory support with the initiation of bilevel positive airway pressure (BiPAP) to improve ventilation and oxygenation. Concurrently, the team re-evaluates his hemodynamic status, opting to adjust the labetalol infusion to maintain a more stable blood pressure within a target range that optimizes cerebral perfusion while minimizing the risk of worsening cerebral edema or hemorrhagic transformation.

This shift in Mr. Thompson’s condition necessitates a comprehensive review of his care plan. The team considers the potential need for more aggressive interventions, such as endotracheal intubation, should his respiratory status continue to decline. They also contemplate the initiation of additional neuroprotective measures, including hypertonic saline, to manage intracranial pressure more effectively. Continuous monitoring for signs of further neurological decline, such as changes in pupil reactivity or additional motor deficits, will be critical in guiding ongoing treatment decisions. The evolving complexity of Mr. Thompson’s case highlights the importance of adaptive clinical reasoning to address both immediate needs and potential future complications.

Section 3

The medical team closely monitors Mr. Thompson's response to the initiation of BiPAP and adjustments to his labetalol infusion. Over the next few hours, there is a slight improvement in his oxygen saturation, which stabilizes around 92-94%. His respiratory rate decreases to a more manageable 24 breaths per minute, suggesting some relief in his labored breathing. However, Mr. Thompson's neurological status continues to be concerning. A repeat neurological assessment reveals that his Glasgow Coma Scale has decreased to 8, with further reduction in his ability to obey commands and open his eyes spontaneously, indicating a potential need for more aggressive intervention.

Concurrent with these observations, new diagnostic results reveal an elevated serum sodium level of 148 mEq/L, reflecting the administration of hypertonic saline aimed at managing intracranial pressure. A follow-up CT scan of the brain shows no new areas of hemorrhage but suggests the presence of diffuse cerebral edema. This finding prompts the clinical team to consider the balance between maintaining adequate cerebral perfusion pressure and preventing further edema. They deliberate on whether to continue with hypertonic saline therapy and BiPAP or commence preparations for endotracheal intubation to secure the airway, especially given the risk of rapid neurological deterioration.

As they weigh these decisions, the team remains vigilant for any new complications that may arise, such as potential electrolyte imbalances or cardiac arrhythmias related to the interventions. Continuous monitoring of Mr. Thompson's vital signs, neurological status, and laboratory parameters will be crucial in guiding the next steps in his care, ensuring that interventions are timely and appropriate to prevent further decline. This approach underscores the necessity of dynamic clinical reasoning to adapt to Mr. Thompson’s evolving clinical picture, ensuring that both immediate and long-term outcomes are optimized.

Section 4

As the clinical team continues to monitor Mr. Thompson, a new complication emerges that requires immediate attention. While his oxygen saturation has stabilized with BiPAP support, his heart rate begins to show irregularities. The telemetry monitor reveals the onset of frequent premature ventricular contractions (PVCs), raising concerns about potential electrolyte imbalances, particularly given his recent hypertonic saline administration and elevated serum sodium levels. A prompt electrolyte panel is ordered, and results indicate a mild hypokalemia with a potassium level of 3.2 mEq/L. This finding necessitates a careful review of Mr. Thompson's fluid and electrolyte management to prevent further cardiac complications.

In response to the PVCs and the risk of arrhythmias, the medical team decides to initiate potassium supplementation while continuing to monitor his cardiac rhythm closely. Adjustments to his intravenous fluids are made to address his electrolyte imbalances without exacerbating his cerebral edema. Additionally, the team considers the need for magnesium levels, given the interdependence of potassium and magnesium in cardiac stability. As these interventions are implemented, the team remains vigilant, understanding the delicate balance required to manage Mr. Thompson's complex condition.

While addressing the cardiac issue, Mr. Thompson's neurological status continues to demand attention. Despite the initial stabilization of his respiratory parameters, his decreased Glasgow Coma Scale score and signs of diffuse cerebral edema necessitate a reevaluation of his airway management. After thorough deliberation, the decision is made to proceed with endotracheal intubation to secure his airway and ensure adequate oxygenation, especially in light of his deteriorating neurological status. This step is taken with the understanding that it will provide better control over his respiratory function and allow for more aggressive management of intracranial pressure, thus optimizing cerebral perfusion. The team's dynamic approach and ongoing assessment are crucial in adapting to Mr. Thompson's evolving needs, reflecting the complexity of his care and the importance of timely intervention.

Section 5

As the clinical team continues to manage Mr. Thompson's condition, a new complication arises that requires immediate attention. Despite the recent efforts to stabilize his cardiac rhythm through potassium supplementation, Mr. Thompson begins to exhibit a change in his neurological status. During the routine neurological assessment, the nurse notes an increase in his pupillary size with a sluggish reaction to light on the left side, accompanied by an increased systolic blood pressure and bradycardia. These signs raise alarms for potential worsening intracranial pressure, prompting an urgent review of his intracranial status. A stat CT scan of the brain is ordered to assess for any progression of cerebral edema or hemorrhagic transformation, which could further compromise his neurological function.

The CT scan reveals an increase in cerebral edema and a slight midline shift, indicating rising intracranial pressure. In response to these findings, the medical team intensifies their management strategy. Mannitol is administered to help reduce the cerebral edema, and the head of Mr. Thompson's bed is elevated to 30 degrees to facilitate venous drainage from the brain. Additionally, the team initiates a hyperosmolar therapy protocol with careful monitoring of serum osmolarity to avoid exacerbating his electrolyte imbalances. These interventions are aimed at optimizing cerebral perfusion pressure and preventing further neurological deterioration.

As Mr. Thompson continues to be closely monitored, the team remains vigilant for any further complications. The complex interplay between his cardiac and neurological issues requires a coordinated, multidisciplinary approach. The nurses and physicians communicate frequently to ensure timely interventions, with a focus on maintaining adequate cerebral perfusion and preventing secondary brain injury. The evolving nature of Mr. Thompson's condition underscores the critical role of continuous assessment and adaptation in providing effective care, highlighting the importance of clinical reasoning in navigating the challenges of his treatment.