A patient with a history of hypertension and diabetes presents with signs of fluid overload, possible atelectasis, and elevated cardiac enzymes. Despite oxygen therapy and nitroglycerin, the patient becomes increasingly restless and confused. What is the priority nursing intervention to address the patient's current condition?

B) Reassess the patient's oxygenation and consider increasing oxygen delivery.

A) Increase the rate of intravenous fluids to improve perfusion.

B) Reassess the patient's oxygenation and consider increasing oxygen delivery.

C) Administer a diuretic to reduce fluid overload.

D) Prepare the patient for an immediate CT angiogram.

A patient with a history of hypertension and diabetes presents with diminished breath sounds, cyanosis, jugular vein distention, and sinus tachycardia. The healthcare team is concerned about potential myocardial ischemia and possible acute kidney injury. After initiating oxygen therapy and nitroglycerin, the patient becomes restless and confused. Which intervention should the nurse prioritize next?

C) Perform a neurological assessment

A) Increase the flow rate of supplemental oxygen

B) Administer a bolus of intravenous fluids

C) Perform a neurological assessment

D) Prepare the patient for a CT angiogram

A patient with multiple small emboli in the right pulmonary artery is on a heparin infusion and has been prescribed a beta-blocker to manage tachycardia. The nurse notes the patient's heart rate remains in the 120s and blood pressure is 165/95 mmHg. Which nursing intervention is most appropriate to address the patient's hemodynamic status?

D) Notify the healthcare provider about the need for additional cardiac support.

A) Increase the heparin infusion rate to reduce clot burden.

B) Administer an additional dose of beta-blocker as prescribed.

C) Position the patient in a high Fowler's position to optimize breathing.

D) Notify the healthcare provider about the need for additional cardiac support.

A patient with a pulmonary embolism is on a heparin infusion and a newly added beta-blocker to manage tachycardia and hypertension. Despite these interventions, the patient continues to exhibit persistent tachycardia and elevated blood pressure. What is the most appropriate nursing intervention to prioritize at this time?

C) Collaborate with the healthcare provider to reassess and potentially adjust the beta-blocker dosage.

A) Increase the rate of the heparin infusion.

B) Administer supplemental oxygen to improve oxygenation.

C) Collaborate with the healthcare provider to reassess and potentially adjust the beta-blocker dosage.

D) Encourage the patient to perform deep breathing exercises to reduce anxiety.

A patient with a pulmonary embolism is experiencing worsening respiratory distress and altered mental status. Arterial blood gas analysis shows a pH of 7.32, PaCO2 of 48 mmHg, and HCO3 of 22 mEq/L. Which nursing intervention is the priority to address the patient's condition?

C) Transition the patient to non-invasive ventilation (NIV).

A) Increase the flow rate of oxygen via nasal cannula.

B) Prepare the patient for endotracheal intubation.

C) Transition the patient to non-invasive ventilation (NIV).

D) Administer a bronchodilator to improve airflow.

A patient with a diagnosed pulmonary embolism and recent changes in neurological status is being monitored in a critical care unit. The nurse notices the patient is increasingly lethargic with a drop in Glasgow Coma Scale score from 15 to 12, and arterial blood gas analysis shows a pH of 7.32, PaCO2 of 48 mmHg, and HCO3 of 22 mEq/L. Which nursing intervention is most appropriate to prioritize at this time?

C) Initiate non-invasive ventilation to support respiratory function

A) Increase the oxygen flow rate on the nasal cannula to 6L/min

B) Prepare the patient for an immediate CT scan of the head

C) Initiate non-invasive ventilation to support respiratory function

D) Administer a sedative to help the patient rest and reduce respiratory distress

A patient with a known pulmonary embolism and new deep vein thrombosis is receiving alteplase therapy. Which nursing intervention is the most critical to prioritize in the first 24 hours of thrombolytic therapy?

A) Monitor neurological status closely for any changes

B) Encourage increased fluid intake to prevent dehydration

C) Educate the patient about the importance of bedrest

D) Assist with ambulation to promote circulation

A patient with worsening pulmonary emboli and a new DVT is being transitioned to a continuous infusion of alteplase and placed on BiPAP. Which assessment finding should the nurse prioritize reporting to the healthcare provider?

C) A blood pressure reading of 90/60 mmHg.

A) An increase in oxygen saturation to 96% with BiPAP support.

B) The patient's Glasgow Coma Scale score remaining at 12.

C) A blood pressure reading of 90/60 mmHg.

D) A heart rate of 118 beats per minute.

A patient with mild cerebral edema is being treated with intravenous mannitol. The nurse notes that the patient's serum lactate levels are elevated, and the patient is experiencing hypotensive episodes. What is the nurse's priority action in managing this patient's care?

B) Administer a bolus of isotonic saline to address hypotension

A) Increase the rate of mannitol infusion to reduce cerebral edema

B) Administer a bolus of isotonic saline to address hypotension

C) Notify the healthcare provider about the elevated lactate levels

D) Monitor fluid balance and renal function closely

A patient with mild cerebral edema is being treated with intravenous mannitol. The nurse observes a rise in serum lactate levels and mild thrombocytopenia. Which nursing intervention is most appropriate to prioritize in this scenario?

C) Monitor renal function closely and assess for signs of fluid overload

A) Increase the rate of mannitol infusion to reduce cerebral edema more rapidly

B) Administer additional anticoagulants to address elevated D-dimer levels

C) Monitor renal function closely and assess for signs of fluid overload

D) Initiate a high-sodium diet to compensate for potential electrolyte imbalances

abnormal vital signs - Nursing Case Study

Pathophysiology

• Primary mechanism: Sympathetic nervous system activation leads to increased heart rate and blood pressure as a compensatory response to stress or hypovolemia, enhancing cardiac output and tissue perfusion.

• Secondary mechanism: Release of catecholamines (e.g., adrenaline) causes vasoconstriction, which can elevate blood pressure but may reduce perfusion to certain tissues, potentially leading to ischemia.

• Key complication: Prolonged sympathetic activation and vasoconstriction can result in organ damage due to sustained hypertension and decreased tissue oxygenation.

Patient Profile

Demographics:

45-year-old male, construction worker

History:

• Key past medical history: Hypertension, Type 2 Diabetes

• Current medications: Lisinopril, Metformin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Shortness of breath and chest discomfort

• Key symptoms: Fatigue, dizziness, intermittent headache

• Vital signs: Blood pressure 160/95 mmHg, heart rate 105 bpm, respiratory rate 22 breaths per minute, temperature 99.1°F, oxygen saturation 92% on room air

Section 1

During the initial assessment, further evaluation of the patient's respiratory status revealed diminished breath sounds in the lower lobes of both lungs, suggesting possible atelectasis or early pulmonary edema due to fluid overload. The patient also exhibited mild cyanosis around the lips and nail beds, consistent with the observed hypoxemia. Notably, the patient's jugular veins were distended, indicating increased central venous pressure, possibly linked to right-sided heart strain or congestive heart failure exacerbation. An electrocardiogram (ECG) showed sinus tachycardia with some nonspecific ST-segment changes, raising concerns about myocardial ischemia in the context of his ongoing chest discomfort.

Given the patient's history of hypertension and diabetes, the healthcare team prioritized obtaining a complete blood count (CBC), basic metabolic panel (BMP), and cardiac enzymes to further evaluate his condition. Initial lab results showed elevated blood glucose levels at 245 mg/dL and increased serum creatinine at 1.9 mg/dL, suggesting potential acute kidney injury possibly due to poor perfusion or the effects of hypertension. Additionally, cardiac troponin levels were slightly elevated, indicating possible cardiac stress or a non-ST elevation myocardial infarction (NSTEMI).

The clinical team initiated supplemental oxygen therapy, raising the patient's oxygen saturation to 95%, and administered nitroglycerin to alleviate chest discomfort and reduce cardiac workload. Despite these interventions, the patient began to exhibit increased restlessness and confusion, which could signify worsening hypoxemia or decreased cerebral perfusion. This change in mental status prompted an urgent review of his treatment regimen and consideration of advanced imaging, such as a CT angiogram, to rule out pulmonary embolism or other acute complications. The unfolding clinical scenario necessitates careful reassessment and adjustment of the management plan to stabilize the patient's condition and prevent further deterioration.

Section 2

In response to the patient's increased restlessness and confusion, the clinical team expedited advanced diagnostic imaging, opting for a CT angiogram to investigate the possibility of a pulmonary embolism. The scan revealed multiple small emboli in the right pulmonary artery, which were contributing to the patient's respiratory distress and hypoxemia. The presence of these emboli was consistent with the patient's elevated central venous pressure and could explain the new onset of altered mental status due to impaired oxygenation. Additionally, laboratory results showed a further elevation in cardiac troponin levels to 0.15 ng/mL, reinforcing concerns of cardiac strain related to the pulmonary embolism.

With these findings, the team adjusted the management plan to include anticoagulation therapy to address the pulmonary embolism. The patient was started on a heparin infusion to prevent further clot formation. However, despite this intervention, the patient continued to exhibit tachycardia, with heart rates persistently in the 120s, and his blood pressure remained elevated at 165/95 mmHg. This sustained cardiovascular strain necessitated closer monitoring and prompted the team to consider additional support for both the cardiac and respiratory systems.

Clinicians also revisited the patient's medication regimen, adding a beta-blocker to help control the heart rate and reduce myocardial oxygen demand. Moreover, the team increased the frequency of neurological assessments to monitor for any further changes in mental status that might suggest worsening cerebral perfusion. These steps aimed to stabilize the patient while addressing the interconnected nature of his cardiac, respiratory, and neurological challenges, setting the stage for ongoing evaluation and adjustment of the therapeutic approach.

Section 3

Despite the initiation of the heparin infusion and the addition of a beta-blocker, the patient experienced a change in status that required immediate attention. Over the next several hours, the patient showed signs of worsening respiratory distress, evidenced by increased work of breathing, use of accessory muscles, and a respiratory rate that climbed to 32 breaths per minute. Pulse oximetry readings dropped to 88% on 4L/min of nasal cannula oxygen, indicating significant hypoxemia. This prompted the clinical team to escalate respiratory support, transitioning the patient to a non-rebreather mask, which temporarily improved oxygen saturation to 94%.

Concurrent with these respiratory changes, the neurological assessments began revealing subtle yet concerning findings. The patient became increasingly lethargic and less responsive to verbal stimuli, requiring physical stimulation to arouse. Pupillary reaction remained intact, but the Glasgow Coma Scale score dropped from 15 to 12, raising alarms about potential cerebral hypoxia or further embolic events affecting cerebral circulation. A repeat CT scan of the head was considered to rule out any acute intracranial pathology, while the team continued to manage the pulmonary embolism aggressively.

The laboratory workup added another layer of complexity; the patient's arterial blood gas analysis showed a pH of 7.32, PaCO2 of 48 mmHg, and HCO3 of 22 mEq/L, indicating a compensated respiratory acidosis. This finding suggested that the patient's respiratory system was struggling to adequately eliminate carbon dioxide, likely due to the increased work of breathing and impaired gas exchange from the emboli. These results, combined with the patient's declining neurological status and persistent cardiovascular strain, underscored the need for a multidisciplinary approach to refine the treatment strategy, potentially considering advanced respiratory support modalities, such as non-invasive ventilation, to stabilize the patient and optimize oxygenation.

Section 4

As the clinical team continued to monitor the patient closely, a new set of diagnostic results revealed further complications. A repeat CT angiogram of the chest showed an increase in the size of the existing pulmonary emboli, accompanied by the development of a small pleural effusion on the right side. This finding explained the patient's persistent hypoxemia and increasing respiratory distress, as the obstruction in pulmonary blood flow had worsened. Additionally, a duplex ultrasound of the lower extremities identified a new deep vein thrombosis (DVT) in the right popliteal vein, suggesting ongoing thromboembolic activity despite the heparin infusion.

In response to these developments, the medical team decided to intensify anticoagulation therapy by transitioning the patient to a continuous infusion of alteplase, a thrombolytic agent, while maintaining close monitoring for any signs of bleeding. Concurrently, the patient's respiratory support was upgraded to BiPAP (Bilevel Positive Airway Pressure) to improve ventilation and reduce carbon dioxide retention, as evidenced by the previous arterial blood gas results. This intervention led to a gradual improvement in the patient's oxygen saturation, which stabilized at 96% with the BiPAP settings adjusted to a pressure support of 10 cm H2O and a positive end-expiratory pressure (PEEP) of 5 cm H2O.

Despite these adjustments, the patient's neurological status remained a concern, as repeat neurological assessments showed no significant improvement in responsiveness. The Glasgow Coma Scale score remained at 12, prompting the team to initiate a neurology consult to evaluate for potential cerebral complications. Meanwhile, the increase in heart rate to 118 beats per minute and a drop in blood pressure to 90/60 mmHg indicated a strain on the cardiovascular system, likely exacerbated by the increased pulmonary vascular resistance. These findings underscored the complexity of the patient's condition, necessitating a coordinated approach across specialties to address the multifaceted challenges and optimize outcomes.

Section 5

As the patient's condition remained precarious, the neurology consult provided new insights into the possible cerebral complications. A CT scan of the brain was conducted, revealing mild cerebral edema but no acute intracranial hemorrhage or infarction. This finding suggested that while there was no immediate cerebral ischemia, the hypoxemic state and potential microembolic events might be contributing to the altered level of consciousness. The neurology team recommended initiating osmotherapy with intravenous mannitol to reduce cerebral edema, in conjunction with continued close monitoring of the patient's neurological status and vital signs.

Simultaneously, the laboratory results indicated a significant rise in the patient's D-dimer levels, now at 5,000 ng/mL (normal <500 ng/mL), reflecting ongoing thrombotic activity. The complete blood count showed a mild thrombocytopenia with platelet levels at 120,000/µL, likely a consequence of both the underlying condition and the intensified anticoagulation therapy. Additionally, serum lactate levels rose to 3.5 mmol/L (normal <2.0 mmol/L), suggesting a state of metabolic stress and possible tissue hypoperfusion, correlating with the patient's hypotensive episodes.

In response to these developments, the multidisciplinary team decided to adjust the treatment plan. They cautiously increased fluid resuscitation with isotonic saline to address the low blood pressure, while being mindful of the risk of exacerbating the pleural effusion. The decision was made to maintain the current thrombolytic regimen due to the high risk of further thromboembolic events, while the patient's renal function was closely monitored to preclude any complications from mannitol administration. These strategic interventions aimed to stabilize the patient’s hemodynamics and support cerebral function, highlighting the necessity for ongoing critical assessment and prompt adaptation to the evolving clinical picture.