A patient in the cardiac care unit is experiencing worsening symptoms of an acute anterior myocardial infarction. The nursing assessment reveals increased chest pain, shortness of breath, crackles at the lung bases, and hypotension after administration of intravenous nitroglycerin. Which nursing intervention is the most appropriate based on these findings?

B) Administer a fluid bolus to address hypotension and support cardiac output.

A) Increase the rate of intravenous nitroglycerin to further alleviate chest pain.

B) Administer a fluid bolus to address hypotension and support cardiac output.

C) Elevate the head of the bed to improve respiratory effort and decrease anxiety.

D) Withhold supplemental oxygen to prevent further drop in blood pressure.

A patient in the cardiac care unit has persistent chest pain despite treatment, hypotension with fluctuating blood pressure, and increasing fatigue and confusion. With a new finding of elevated serum creatinine and BUN, which nursing intervention is most important to prioritize?

B) Monitor urine output hourly to assess renal function.

A) Increase the dose of intravenous nitroglycerin to relieve chest pain.

B) Monitor urine output hourly to assess renal function.

C) Administer a bolus of intravenous fluids to improve blood pressure.

D) Prepare the patient for immediate hemodialysis to address acute kidney injury.

A patient in the cardiac care unit is experiencing persistent chest pain, hypotension, and confusion. Despite treatment with IV nitroglycerin and supplemental oxygen, the symptoms persist. Blood pressure fluctuates between 88/58 mmHg and 92/60 mmHg, and the ECG continues to show ST-segment elevation. The healthcare team decides to initiate low-dose norepinephrine. What is the primary rationale for administering norepinephrine in this scenario?

B) To increase systemic vascular resistance and improve blood pressure.

A) To directly relieve chest pain by enhancing coronary blood flow.

B) To increase systemic vascular resistance and improve blood pressure.

C) To decrease myocardial oxygen demand and reduce cardiac workload.

D) To correct metabolic acidosis by improving renal perfusion.

A patient with acute coronary syndrome and renal impairment is experiencing hypokalemia with a potassium level of 3.2 mEq/L. The healthcare team initiated potassium replacement therapy. Which nursing intervention is most critical to prioritize during this therapy?

C) Monitor cardiac rhythm continuously for any changes.

A) Monitor the patient's blood glucose levels hourly.

B) Assess the patient's urine output every hour.

C) Monitor cardiac rhythm continuously for any changes.

D) Obtain a daily weight to monitor fluid status.

A patient with acute coronary syndrome is experiencing hypokalemia with potassium levels at 3.2 mEq/L and has shown a decreased level of consciousness with a Glasgow Coma Scale score of 13. Which nursing intervention should be prioritized to address these findings?

B) Administer potassium replacement therapy as ordered and monitor cardiac rhythm.

A) Increase the dose of norepinephrine to improve blood pressure and cerebral perfusion.

B) Administer potassium replacement therapy as ordered and monitor cardiac rhythm.

C) Prepare the patient for a CT scan to rule out acute intracranial events.

D) Initiate seizure precautions due to the decreased level of consciousness.

A patient with myocardial ischemia is exhibiting frequent premature ventricular contractions (PVCs) and a brief episode of ventricular tachycardia despite potassium replacement therapy. What is the most appropriate nursing action to address this cardiac instability?

B) Notify the cardiologist to consider magnesium supplementation.

A) Administer an additional dose of potassium chloride as ordered.

B) Notify the cardiologist to consider magnesium supplementation.

C) Increase the rate of norepinephrine infusion to stabilize blood pressure.

D) Prepare the patient for immediate cardioversion to address the PVCs.

A patient with ongoing myocardial ischemia and electrolyte imbalances is being monitored for cardiac instability. Despite potassium replacement therapy, the patient exhibits frequent PVCs and a brief episode of ventricular tachycardia. The cardiologist decides to add magnesium supplementation. What is the primary rationale for adding magnesium in this clinical scenario?

C) Magnesium plays a role in stabilizing cardiac membrane potentials, reducing the risk of arrhythmias.

A) Magnesium helps to directly stabilize blood pressure and improve cerebral perfusion.

B) Magnesium supplementation can enhance the effectiveness of norepinephrine in managing hypotension.

C) Magnesium plays a role in stabilizing cardiac membrane potentials, reducing the risk of arrhythmias.

D) Magnesium reduces the risk of intracranial events by directly affecting the cerebral vasculature.

A patient with a history of cardiac issues has been treated with intravenous furosemide for pulmonary edema and is now showing signs of electrolyte imbalance. Which nursing intervention should be prioritized to prevent further complications?

C) Monitor the patient's respiratory status and oxygen saturation closely.

A) Increase the rate of norepinephrine infusion to counteract hypotension.

B) Administer a potassium supplement to address potential hypokalemia.

C) Monitor the patient's respiratory status and oxygen saturation closely.

D) Encourage the patient to increase oral fluid intake to prevent dehydration.

A patient with a recent adjustment in electrolyte supplementation is showing signs of pulmonary congestion and requires careful management of fluid status. Which nursing intervention is most appropriate to prioritize in this situation?

B) Implement strict input and output monitoring to guide diuretic therapy.

A) Increase the rate of norepinephrine infusion to improve cardiac output.

B) Implement strict input and output monitoring to guide diuretic therapy.

C) Encourage deep breathing exercises to increase oxygen saturation.

D) Administer additional potassium supplementation to stabilize cardiac rhythms.

CAD - Nursing Case Study

Pathophysiology

• Primary mechanism: Atherosclerosis - The buildup of plaque (cholesterol, fatty substances, and cellular waste) in coronary arteries reduces blood flow, leading to ischemia. This process begins with endothelial injury and inflammation, promoting lipid accumulation and plaque formation.

• Secondary mechanism: Endothelial dysfunction - Damage to the inner arterial lining impairs its ability to produce nitric oxide, a vasodilator. This dysfunction contributes to vasoconstriction, further limiting blood supply to the heart muscle and exacerbating ischemic conditions.

• Key complication: Myocardial infarction - When a plaque ruptures, it can form a clot that completely obstructs blood flow, causing heart muscle tissue to die due to prolonged ischemia. This leads to significant cardiac dysfunction and potential heart failure.

Patient Profile

Demographics:

58-year-old male, construction worker

History:

• Key past medical history: Hypertension, Type 2 Diabetes Mellitus, Hyperlipidemia

• Current medications: Metoprolol, Atorvastatin, Metformin, Aspirin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Chest pain and shortness of breath

• Key symptoms: Fatigue, dizziness, intermittent palpitations

• Vital signs: Blood pressure 150/95 mmHg, heart rate 105 bpm, respiratory rate 22 breaths per minute, temperature 98.6°F, oxygen saturation 93% on room air

Section 1

As the patient was admitted to the cardiac care unit, initial assessment findings indicated worsening symptoms. The patient's chest pain increased in intensity and was described as crushing, radiating to the left arm and jaw. Simultaneously, the shortness of breath became more pronounced, with the patient exhibiting increased respiratory effort and anxiety. On auscultation, crackles were noted at the lung bases, suggesting the onset of pulmonary congestion, likely due to left ventricular dysfunction.

Laboratory tests revealed elevated cardiac biomarkers, with Troponin I levels markedly increased at 1.5 ng/mL (normal <0.04 ng/mL), confirming myocardial injury. An electrocardiogram (ECG) showed ST-segment elevation in the anterior leads, indicative of an acute anterior myocardial infarction. Additionally, the patient's blood glucose was elevated at 250 mg/dL, reflecting poor glycemic control likely exacerbated by stress and acute illness.

In response to these findings, the healthcare team promptly initiated treatment with intravenous nitroglycerin to alleviate chest pain and improve coronary blood flow. Supplemental oxygen was administered to maintain adequate oxygenation. Despite these interventions, the patient developed hypotension, with blood pressure dropping to 90/60 mmHg, necessitating careful titration of medications and consideration of further invasive measures, such as percutaneous coronary intervention, to restore perfusion and stabilize the patient's condition. These developments underscore the complexity of managing acute coronary syndrome in the context of multiple comorbidities, requiring diligent monitoring and adjustment of therapeutic strategies to address evolving complications.

Section 2

As the patient continued to receive treatment in the cardiac care unit, new complications arose. Despite the administration of intravenous nitroglycerin and supplemental oxygen, the patient's chest pain persisted, albeit with slightly reduced intensity. The hypotension remained a concern, with blood pressure readings fluctuating between 88/58 mmHg and 92/60 mmHg. The patient exhibited increasing levels of fatigue and confusion, raising concerns about cerebral perfusion. A repeat electrocardiogram (ECG) still showed significant ST-segment elevation, indicating that myocardial ischemia was ongoing and that the initial interventions had not fully resolved the coronary occlusion.

Further diagnostic results revealed a new complication: the patient's renal function had deteriorated, with serum creatinine rising to 2.1 mg/dL from a baseline of 1.0 mg/dL, and blood urea nitrogen (BUN) increasing to 35 mg/dL. This suggested acute kidney injury, potentially secondary to decreased perfusion and the effects of medication. The elevated blood glucose levels persisted, with a current reading of 260 mg/dL, indicating a need for tighter glycemic control as part of the overall management plan.

In light of these developments, the healthcare team decided to initiate low-dose norepinephrine to stabilize blood pressure and maintain adequate organ perfusion. Continuous monitoring of cardiac and renal function was prioritized, with plans to consult nephrology for further evaluation of the renal impairment. The decision was made to proceed with percutaneous coronary intervention (PCI) as soon as possible to address the persistent coronary artery blockage and prevent further myocardial damage. This comprehensive approach highlights the complexity of managing acute coronary syndrome in the presence of multiple complications, emphasizing the need for ongoing reassessment and adaptation of the treatment plan to respond to the patient's dynamic clinical status.

Section 3

As the healthcare team continued to closely monitor the patient, new diagnostic results provided further insight into the evolving clinical picture. The latest laboratory tests revealed an electrolyte imbalance, with potassium levels dropping to 3.2 mEq/L, which raised concerns about the potential for cardiac arrhythmias, particularly given the continued myocardial ischemia. This hypokalemia was likely exacerbated by the initiation of norepinephrine and diuretics used in the management of acute coronary syndrome and renal impairment. In response, the team initiated potassium replacement therapy to correct the imbalance while maintaining vigilant cardiac monitoring.

Additionally, the patient's confusion worsened, and a neurological assessment indicated a decreased level of consciousness, with a Glasgow Coma Scale score dropping to 13. The persistent hypotension and the new electrolyte disturbances likely contributed to decreased cerebral perfusion, necessitating urgent attention. The team considered the potential for metabolic disturbances or further cerebrovascular complications and ordered a CT scan of the head to rule out any acute intracranial events.

Meanwhile, the patient's hemodynamic status remained delicate, with blood pressure readings showing only marginal improvement despite norepinephrine support. To address the ongoing ischemia, plans for the percutaneous coronary intervention (PCI) were expedited. The goal was to restore coronary blood flow and improve overall organ perfusion, which would be critical in stabilizing the patient’s cardiac and renal function and preventing further neurological decline. This strategic move underscored the importance of timely intervention in the face of complex, multifaceted challenges, highlighting the need for coordinated, multidisciplinary care in managing such high-risk cases.

Section 4

As the healthcare team continued to monitor the patient, a significant change in status was observed. Despite the potassium replacement therapy, the patient developed increasing signs of cardiac instability. The telemetry monitor displayed frequent premature ventricular contractions (PVCs), and a brief episode of ventricular tachycardia was noted. This development underscored the precarious balance of the patient’s electrolytes and the critical nature of maintaining potassium levels within normal limits, particularly in the context of ongoing myocardial ischemia and norepinephrine use. The nursing team promptly notified the cardiologist, who adjusted the potassium replacement regimen and considered the addition of magnesium supplementation to further stabilize the cardiac membrane potential.

Concurrently, the patient’s neurological status showed no signs of improvement, with the Glasgow Coma Scale score remaining at 13, prompting the team to review the results of the CT scan. Fortunately, the scan returned negative for acute intracranial events, ruling out conditions such as a hemorrhagic stroke. However, the persistent confusion and decreased level of consciousness continued to raise concerns about cerebral hypo-perfusion as a possible consequence of the persistent hypotension and electrolyte imbalance. With the CT scan findings in hand, the team decided to increase the frequency of neurological checks and maintain strict blood pressure monitoring to optimize cerebral perfusion.

These changes in the patient's status highlighted the intricate interplay between cardiac, renal, and neurological systems, demanding vigilant, coordinated care. The focus remained on stabilizing the patient through the upcoming percutaneous coronary intervention, which was anticipated to relieve myocardial ischemia and ultimately contribute to improved cerebral and systemic perfusion. The healthcare team’s efforts were concentrated on minimizing complications, closely monitoring vital signs, and adjusting therapeutic interventions as needed to navigate the complexities of this challenging clinical picture.

Section 5

In the hours following the adjustments to the potassium and magnesium supplementation, the patient’s cardiac status showed marginal improvement. The telemetry monitor indicated a reduction in the frequency of premature ventricular contractions, and no further episodes of ventricular tachycardia were observed. However, new complications arose as the patient began to exhibit signs of pulmonary congestion. Auscultation revealed bilateral crackles at the lung bases, and oxygen saturation readings began to trend downward, dipping to 88% on room air. The patient's respiratory rate increased to 24 breaths per minute, and mild use of accessory muscles was noted, suggesting the onset of acute heart failure exacerbation likely triggered by fluid overload secondary to aggressive electrolyte replacement.

A repeat chest X-ray confirmed the presence of pulmonary edema. Concerned about the potential for further respiratory compromise, the healthcare team initiated a diuretic therapy regimen, carefully balancing the need to reduce fluid overload with the risk of exacerbating the patient's already unstable electrolyte levels. Lasix (furosemide) was administered intravenously, and strict input and output monitoring was implemented to prevent dehydration or further electrolyte disturbances.

Meanwhile, the patient's neurological status remained unchanged, compounding the complexity of the case. The team decided to implement a low-dose norepinephrine infusion to support blood pressure and improve cerebral perfusion, while continuing frequent neurological assessments. This development underscored the delicate equilibrium required in managing the interconnected cardiac, renal, and neurological challenges. Each intervention was meticulously evaluated for its impact on the patient's overall status while preparing for the upcoming percutaneous coronary intervention. The team's coordinated efforts aimed to stabilize the patient's condition and minimize complications through meticulous monitoring and timely adjustments to the therapeutic strategy.